In support of programmed effects on adipose function in PCOS, we previously have shown that SC abdominal ASCs from eight normal-weight PCOS by NIH criteria versus eight age- and BMI-matched control women cultured without androgen exhibit increased ASC commitment to preadipocytes that negatively correlates with circulating fasting glucose levels, while enhanced lipid accumulation in newly, in vitro-formed adipocytes positively correlates with circulating androgen levels, implying a cellular programmed mechanism to maintain glucose-insulin homeostasis when fat accretion is accelerated [25]. The gene discussed is INS; the disease is polycystic ovary syndrome.