As we find that all hormonal, reproductive, and metabolic alterations of PAMH F1 offspring are maintained in the third generation, we cannot exclude that AMH fetal-determined changes in epigenetic marks, in combination with the recurring high testosterone levels and perhaps with the metabolic disturbances of the PAMH lineage may be the programing agents responsible for the acquisition and transmission of PCOS-like traits through modifications of DNA methylation landscapes. The gene discussed is AMH; the disease is polycystic ovary syndrome.