Importantly, the availability of Alx3-deficient mice on a pure C57BL/6J background allowed us to determine that these mice do not exhibit hyperglycemia or glucose intolerance, but retain increased adiposity and decreased muscle mass and strength (Supplementary Fig. 7), indicating that the muscle phenotype is unrelated to dysfunctional glucose homeostasis. The gene discussed is ALX3; the disease is Glucose intolerance.