Finally, data on the bacterial protein C1pB (produced by both commensal and pathogenic microorganisms) as a mimetic of α-MSH and its effects on activating host satiety pathways in rodents [47], as well as the elevated plasma concentration of anti-C1pB IgG that is cross-reactive with α-MSH in patients with eating disorders [48], accord with the notion that autoantibody-induced interference with the central melanocortin system is one of the key microbiota–gut–brain mechanisms that contributes to dysregulated appetite control in eating disorders. Here, STAMBP is linked to eating disorder.