For example, allele-specific deficiency of imprinted guanine nucleotide-binding protein, α-stimulating (GNAS) gene products led to various metabolic phenotypes: obesity and hypometabolic states (in maternal knockout of Gsα, or Gnas) and leanness with increased metabolic rate (in paternal knockout of XLαs, or Gnasxl) [5,6,7]. Here, GNAS is linked to obesity due to melanocortin 4 receptor deficiency.