Somewhat to our surprise, mice carrying a homozygous deletion of Gαs in SF1‐expressing cells of the VMH (VMHGsKO) showed no alterations in body weight or food intake when raised under SCD or HFD feeding conditions.[83] This result might be due to the crosstalk between stimulatory and inhibitory G protein α subunits to compensate for the deletion of Gαs protein.[84, 85, 86] It is also possible that Gαs and AC3 are distributed in different cell types within the VMH and exert different physiological functions in body weight regulation. The gene discussed is ADCY3; the disease is Schnyder corneal dystrophy.