LepRb neuron‐specific ablation of Sh2b1 abrogates the ability of leptin to stimulate sympathetic nerve activity, suppresses brown adipose tissue (BAT) thermogenesis, and causes obesity, insulin resistance, and MASLD.[12] Unexpectedly, food intake is normal in the mutant mice; hence, SH2B1 neurons, which regulate appetite, remain unknown. Here, SH2B1 is linked to metabolic dysfunction-associated steatotic liver disease.