TrkB receptors are expressed in hypothalamic nuclei and seem to be involved in the regulation of mammalian eating behavior and energy balance.5,6 Moreover, a heterozygous de novo mutation in the NTRK2 causing a loss of function has previously been shown in a patient with early-onset obesity, hyperphagia, and severe developmental delay.7,8 Activation of BDNF/TrkB signaling reduces food intake and body weight gain as BDNF acts as a catabolic agent. The gene discussed is NTRK2; the disease is obesity due to melanocortin 4 receptor deficiency.