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. Here, SF1 is linked to Schnyder corneal dystrophy.