Polycystic ovary syndrome (PCOS) is one of the most common, yet heterogeneous and complex, endocrine disorders in women of reproductive age. Although the aetiology of PCOS remains uncertain, emerging evidence has indicated that exposure of the female fetus to the hyperandrogenism milieu in utero may result in PCOS phenotype after birth. Such a phenomenon has been formulated as the fetal origin of PCOS, which intends to give a possible explanation for PCOS aetiology. Given that the epigenetic modifications are usually involved in the development and inheritance of many adult diseases with fetal origin, we propose a hypothesis here referred to as "epigenetic abnormality underlying the fetal origin of PCOS". It states that in utero hyperandrogenism exposure may disturb the epigenetic reprogramming in fetal reproductive tissue, thereby resulting in postnatal POCS phenotype in women of reproductive age. Meanwhile, the incomplete erasure of such epigenetic abnormality in germ cells after fertilization may promote the transgenerational inherence of POCS. Thus, this epigenetic abnormality hypothesis has established a novel mechanism for PCOS development and inheritance. If verified, our hypothesis would open new avenues for the possible intervention at the critical period of prenatal life to prevent PCOS development and inheritance in adult women. Moreover, analysis of the epigenetic phenotypes and identification of specific epigenetic changes may help develop new tools for monitoring fetal development under an in utero hyperandrogenism environment.