For example, we found that anaplastic lymphoma kinase (Alk) expression was down-regulated in CeLNTS/Tac2 neurons in fasted mice (Fig. 7D), a gene whose genetic deletion was previously shown to result in thin animals with resistance to diet- and leptin mutation–induced obesity, acting mainly in the hypothalamus (70). This evidence concerns the gene ALK and obesity due to melanocortin 4 receptor deficiency.