A general DNA methylome profiling of GCs recently has revealed an altered methylation in genes regulating pivotal ovarian functions in PCOS [66]: in particular, few differentially methylated genes, including aldo-keto reductase family 1 member C3, calcium-sensing receptor, growth hormone-releasing hormone receptor and tumor necrosis factor, which predominantly contribute to hyperandrogenism, premature luteolysis and oocyte development defects, can be explored as novel epigenetic candidates in mediating ovarian dysfunction. Here, CASR is linked to hyperandrogenism.