The well-controlled LH levels during COH by CC, particularly the reduced occurrence of premature LH elevation in women with obesity and normal menstrual cycles, can be attributed to several potential mechanisms: [1] Impaired hypothalamic-pituitary responses during COH in individuals with obesity may result from obesity-induced insulin resistance, elevated levels of inflammatory factors and leptin, as well as decreased endogenous kisspeptin secretion (37, 38). The gene discussed is PLOD1; the disease is obesity due to melanocortin 4 receptor deficiency.