Preclinical studies demonstrate that maternal HFD exposure sex-dependently reprograms arcuate nucleus circuitry: Male offspring exhibit amplified orexigenic signaling through increased AgRP neuron populations, elevated AgRP-to-POMC neuron ratios, and expanded arginine vasopressin/retinoic acid receptor-related orphan receptor β (Avp/Rorb) neuronal clusters, collectively driving hyperphagia and insulin dysregulation that predisposes them to obesity [177]. The gene discussed is POMC; the disease is obesity due to melanocortin 4 receptor deficiency.