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(A) A hypothetical model of finasteride acting as an endocrine disruptor. Finasteride via inhibiting key neuro-steroid biosynthesis promotes epigenetic changes in gene expression leading to silencing or attenuating physiological responses. Inhibition of 5a-reductases activities by the high affinity, slow dissociating inhibitor (finasteride) results in depleting the substrate precursors for the 3a-hydroxy-steroid dehydrogenases and therefore blocking biosynthesis of neuro-steroids. This inhibition results in attenuating the function of neurotransmitter receptors and promotes changes in the expression of a host of gene products, thus eliciting epigenetic changes manifested in histone acetylation, methylation, and DNA methylation and upregulation of androgen receptor (AR) gene expression. These changes together with depleted neurosteroid pool manifest itself in the development of PFS in susceptible individuals. (B) The epigenetic changes induced by finasteride elicited endocrine disruption, illustrated in a, produce pathophysiological changes that are manifested as constellations of symptoms of PFS. (Adapted, with permission from the publisher, from Traish AM. The post-finasteride syndrome: clinical manifestation of drug-induced epigenetics due to endocrine disruption. Current Sexual Health Reports 2018;10(3):88–103.)