Our results suggested that KIDINS220/ARMS, through sustaining the phosphorylation of extracellular signal-regulated kinase (ERK), could function as a negative regulator for the adipocyte differentiation, thus the truncated mutation of KIDINS220/ARMS could lead to uncontrolled differentiation and maturation of adipose cells, which caused obesity in SINO patients. The gene discussed is KIDINS220; the disease is obesity due to melanocortin 4 receptor deficiency.