Thus smoking could influence the pathogenesis of prostate cancer via the epigenetic dysregulation of CYP1A1. The putative mechanisms underlying tobacco smoking and regulation of CYP1A1 methylation is that smoking promotes AhR/ARNT heterodimer binding to XREs which leads to loss of methylation by eliminating DNA methyltransferases from the CYP1A1 enhancer [19]. This evidence concerns the gene AHR and Familial prostate cancer.