<p>Polycystic ovary syndrome (PCOS) is a leading cause of anovulatory infertility. Owing to its heterogeneity and multifactorial nature, the aetiology of this disorder remains enigmatic.&#xa0;Recent progress in high-throughput sequencing and molecular biology methods highlights the combined impact of genetic and epigenetic influences on the development of PCOS. Moreover, the absence of clear genetic risk factors, along with growing evidence for the significance of intrauterine and lifestyle influences, provides strong support for the epigenetic model in the inheritance and pathogenesis of PCOS. Alterations in DNA methylation, histone modification and regulation of non-coding RNAs contribute to altered epigenome landscape in PCOS. Recently, modifications to RNA are emerging as new regulator of gene expression. N6-methyladenosine (m6A), is the most common and prevalent modification on mRNA. m6A methylation is reported to regulate mRNA stability, splicing, and translation of genes essential for oocyte and follicular development. A few investigations have reported altered levels of m6A methylation and its regulatory proteins in granulosa cells of women with PCOS as well as in ovarian tissues of animal models of PCOS. These molecular alterations have been linked to increased immune cell infiltration, hyperandrogenism, and impaired oocyte maturation. This review summarizes the functional dynamics of m6A modification, the roles of its regulatory proteins, and its physiological significance in folliculogenesis, highlighting how disruptions in this process may contribute to the PCOS pathophysiology.</p>