In addition to MMU2, three other congenics (HG9, HG11 and HG17) captured hg modifier QTL. In classical terms, they are QTL which modify the expressivity of growth and obesity in HG mice [18]. These QTL are novel since they represent epistasis between hg and the modifier gene. QTL-hg epistasis implies that Socs2 and the hg modifiers are in the same biological pathway. Therefore, these QTL are likely due to polymorphism in genes interacting with Gh, responsive to Gh or which in some way modulate Gh function. This information will significantly aid QTL cloning by providing another filter to screen candidates. Cloning these QTL has major implications to improve our understanding of Gh and its regulation of growth and adiposity and in the administration of human Gh therapeutics.