Although homeostatic responses for maintenance of euglycemia and normal blood pressure are well accepted within the scientific and medical communities and, indeed, form the physiologic basis of our current pharmacologic management of diabetes (e.g., insulin, metformin, and sodium–glucose cotransporter 2 inhibitors) and hypertension (e.g., diuretics, beta‐blockers, and angiotensin convertase enzyme inhibitors), such understanding is less intuitive for adipose mass regulation, especially in the care of patients with the disease of obesity (Fig. 1). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.