AR recruits DNMT1 and the histone-methyltransferase EZH2 to target promoters, accelerating hyper-methylation and H3K27me3 deposition on tumor-suppressor genes (Zimmerman et al., 2023); pharmacological or genetic AR blockade in the N-butyl-N-(4-hydroxybutyl) -nitrosamine (BBN) mouse model attenuates both methylation drift and tumor incidence (Doshi et al., 2023). The gene discussed is DNMT1; the disease is neoplasm.