Altogether, this lends support to an alternate model, in which hyperinsulinemia may act as an early defect in PCOS pathogenesis that precedes the impairment of insulin-induced glucose disposal, perhaps in a subset of the metabolically perturbed lean or obese patients who have been proposed to have a metabolic clinical onset of PCOS (Rotterdam phenotypes A-C; Table 1; Dapas et al. 2020, Unfer et al. 2024). The gene discussed is INS; the disease is hyperinsulinism.