The sparse attention paid in published human reports to the natural history of NAFLD in human monogenic obesity is likely to be attributable to the rarity of the diseases, to the fact that most patients identified are children in whom clinically overt liver NAFLD has not yet had time to develop and to that fact that, in leptin deficiency, curative therapy with recombinant human leptin is the standard of care. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.