LEPR and obesity disorder: While the constitutive disruption of LepR signaling leads to hyperphagia and obesity in humans and animal models3, and knockout of Lepr in LH increases food intake35,36, LepRLH-specific neural activity manipulations in animal models provide a more multifaceted perspective—whereas activation of LepRLH neurons in sated animals in a familiar environment has little effect on food intake6,37–39, activation of LepRLH neurons in hungry animals decreases food intake6, revealing state-dependent regulation of feeding behavior by LepRLH neurons.