A new article published in Biomedicine Pharmacotherapy reported a key role for the transcription factor PAX6 in the modulation of polycystic ovarian syndrome PCOS induced endometrial epithelial proliferation. This article elaborated that PAX6 was significantly induced in the endometrial tissues from PCOS patients and this induction regulated upstream by high levels of insulin was closely correlated to the pathogenesis of insulin resistance IR in endometrial epithelial cells. Overexpression of the exogenous PAX6 potentiated the insulin elicited accumulation of S phase in endometrial epithelial cells and thereby promoted endometrial epithelial proliferation. It was demonstrated that on using luciferase reporter and ChIP assay PAX6 directly bound to the promoter of CDKN1B gene the gene encoding p27 protein a negative regulator of cell cycle and inhibited CDKN1B transcription in the insulin stimulated endometrial epithelial cells. Thus it was concluded that excessive PAX6 expression in insulin challenged endometrial epithelial cells may contribute to the uncontrollable endometrial epithelial proliferation. The findings conferred a mechanistic explanation for the functional link between hyperinsulinemia and p27 loss in the pathogenesis of endometrial epithelial hyperplasia in PCOS patients.