HDAC10
histone deacetylase 10
Theoretical — per Powers
Gene summary
A protein-coding gene on chromosome 22 (epigenetic regulation). The protein encoded by this gene belongs to the histone deacetylase family, members of which deacetylate lysine residues on the N-terminal part of the core histones. Histone deacetylation modulates chromatin structure, and plays an important role in transcriptional regulation, cell cycle progression, and developmental events.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
Polyamine deacetylase HDAC10
- Function
Polyamine deacetylase (PDAC), which acts preferentially on N(8)-acetylspermidine, and also on acetylcadaverine and acetylputrescine. Exhibits attenuated catalytic activity toward N(1),N(8)-diacetylspermidine and very low activity, if any, toward N(1)-acetylspermidine. Histone deacetylase activity has been observed in vitro. Has also been shown to be involved in MSH2 deacetylation. The physiological relevance of protein/histone deacetylase activity is unclear and could be very weak. May play a role in the promotion of late stages of autophagy, possibly autophagosome-lysosome fusion and/or lysosomal exocytosis in neuroblastoma cells. May play a role in homologous recombination. May promote DNA mismatch repair.
- Subcellular location
Cytoplasm; Nucleus.
- Tissue specificity
Widely expressed with high levels in liver and kidney.
Source: UniProtKB/Swiss-Prot Q969S8, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.
Why its pathway is in the library
Epigenetic persistence is the leading hypothesis for why post-drug syndromes endure after the drug is gone; chromatin regulators are therefore priority candidates in any persistence mechanism.
Written for the whole epigenetic regulation family, not for HDAC10 specifically.
Powers’ note (his unpublished theorizing)
Named by Powers (2026 summit interview, unpublished): among epigenetic-monitoring genes showing recurring “glitches” in whole-genome sequencing of ~100 PFS patients; he theorizes failed removal of epigenetic flags after drug discontinuation.
Narrative library record
Function
Class IIb histone deacetylase that removes acetyl groups from lysine residues on core histones (and polyamines such as N8-acetylspermidine), producing a tag for epigenetic repression; acts in large multiprotein complexes to regulate transcription, cell-cycle progression, and development.
Corpus relevance
Third of Powers' recurring genome hits (iWFDBRTgT3g). A histone deacetylase is a natural fit for the corpus's epigenetic models - Traish's drug-induced epigenetics (PFS-002), patient fasting/HDAC experiments discussed on r/DrWillPowers (DWP-007), and Powers' own castration-trial framing all orbit histone-modification biology. Attribution: theoretical-per-Powers (unpublished interview claim).
- YT-iWFDBRTgT3gDr. Will Powers Interview [PFS / PAS / PSSD Summit 2026]
- PFS-002The post-finasteride syndrome: clinical manifestation of drug-induced epigenetics due to endocrine disruption
- DWP-002Untitled long-form research update — new model of PFS/PSSD/post-drug syndromes (Sept 2026)
- DWP-007PFS/PSSD: I'm going to try something interesting…
Powers’ claims naming HDAC10
- Powers gene claim
ARID1A; CHD8; HDAC10 — recurring "glitches" (unspecified)
Confidence: interview
In whole-genome sequencing of ~100 PFS patients, glitches in epigenetic monitoring genes — ARID1A, CHD8, HDAC10 — appear "more than they should" statistically. Epigenetic flags (e.g., for AR upregulation) may fail to be removed after drug discontinuation.
ARARID1ACHD8HDAC10PGL-ARID1A-CHD8-HDAC102026-04-29PFS
Mentioned in 9 corpus records
- Video
Dr. Will Powers Interview [PFS / PAS / PSSD Summit 2026]
Dr. Will Powers · SIDEfxHUB - PFS & PSSD Patient Organisation · 21:27 (1287s)
PFS, PAS, PSSD mechanism theory; Powers' unifying model; vulnerability screening
ARARID1ACHD8HDAC10YT-iWFDBRTgT3g2026-04-29PFSPSSDPRSDCore corpus - Timeline event
Richest primary source on his mature model: androgen-metabolism genomes 'broken at baseline,' glucuronidation-defect selection bias, three phenotypes (neurosteroid vs androgenic-silencing), window/crash dynamics, chemical-castration trials, epigenetic genes…
ARID1ACHD8HDAC10TL-2026-04-29-powers-summit-interview-uploaded-recorded-at-2026-pfs2026-04-29PFSPSSDPRSDCore corpus - Powers · Reddit commentCurated Powers pick
Re: Questions regarding current PFS theory
u/drwillpowers · r/DrWillPowers
Answering questions about variable onset and post-cessation crashes, Powers gives three linked explanations. First, milder or slower onsets reflect fewer defects — it takes longer to reach threshold. Second, people who crash on quitting had upregulated…
ARID1ACHD4CHD5CHD6CHD7+3PRH-15012026-04-18T08:57:02ZPFSPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: Im going to be taking the week off next week to…
u/drwillpowers · r/DrWillPowers
Replying to a post-letrozole case with PFS-identical symptoms (a Klinefelter patient), Powers frames PFS and PSSD as the same mechanism in different flavors — inborn metabolic error plus drug, with recovery blocked by an epigenetic glitch — and notes…
ARID1AHDAC10KDM6APRH-15042026-04-19T00:13:31ZPFSPSSDPowers Reddit history - Glossary term
HDAC (histone deacetylase)
epigenetic
Enzymes that remove acetyl groups from histones, typically silencing genes. The corpus mentions HDACs two ways: fasting-induced beta-hydroxybutyrate acts as an HDAC inhibitor (patient experiment, DWP-007), and HDAC10 recurs among genes Powers reports in PFS…
HDAC10GL-hdacPFSCore corpus - Glossary term
ARID1A / CHD8 / HDAC10
epigenetic
Chromatin-remodeling/epigenetic-regulator genes that Powers reports recurring across PFS patient genomes in his summit interview — offered as candidate genetic-susceptibility loci for post-drug syndromes, pending formal publication.
ARID1ACHD8HDAC10GL-arid1a-chd8-hdac10PFSCore corpus - Gene recordPowers’ theory
Core DNA-binding subunit of the mammalian SWI/SNF (BAF) chromatin-remodeling complex; uses an ARID domain to bind AT-rich DNA and targets the remodeling complex to chromatin, regulating transcription, DNA repair, and differentiation. Frequently mutated in…
ARARID1ACHD8HDAC10GENE-ARID1APFSCore corpus - Gene recordPowers’ theory
ATP-dependent chromatin-remodeling enzyme of the CHD family (SNF2-like ATPase plus chromodomains); regulates transcription both up and down depending on recruited cofactors, interacting with beta-catenin/Wnt signaling, p53, CTCF, and histone-methylation…
ARID1ACHD8CTCFHDAC10GENE-CHD8PFSCore corpus - Gene recordPowers’ theory
Rate-limiting enzyme of folate metabolism that converts 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the methyl donor for remethylating homocysteine to methionine and ultimately producing S-adenosylmethionine - the universal methyl donor for…
ARID1ACHD8HDAC10MTHFRGENE-MTHFRPFSCore corpus
Also in epigenetic regulation
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chr 14· Epigenetic regulation· 9 records - CHD4
chromodomain helicase DNA binding protein 4
chr 12· Epigenetic regulation· 1 record - CHD5
chromodomain helicase DNA binding protein 5
chr 1· Epigenetic regulation· 1 record - CHD6
chromodomain helicase DNA binding protein 6
chr 20· Epigenetic regulation· 1 record - CHD7
chromodomain helicase DNA binding protein 7
chr 8· Epigenetic regulation· 1 record - CHD9
chromodomain helicase DNA binding protein 9
chr 16· Epigenetic regulation· 1 record - CREBBP
CREB binding lysine acetyltransferase
chr 16· Epigenetic regulation· 1 record
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