Therefore the lack of any overt obesity phenotype in Tyto alba despite the homozygous H9P β-MSH loss of function mutation might be explained by compensation through serine amplification to 10–24 residues in the γ3-MSH locus, diminishing cleavage of POMC at site 2 and increasing the levels of γ3-MSH, in analogy to rodents. Here, POMC is linked to obesity disorder.