Recent research has shown that CpG hypomethylation regarding GHRHR, AKR1C3, RETN, and MAMLD1 and hypermethylation regarding TNF, which can indirectly contribute to androgen excess, were consistent with increased and decreased levels of the corresponding gene transcripts, respectively (Sagvekar et al., 2019). This evidence concerns the gene MAMLD1 and hyperandrogenism.