Genetic deletion of Ip6k1 or Ip6k3 or pharmacologic disruption of IP6Ks protects mice from metabolic diseases including obesity, type-2 diabetes (T2D), non-alcoholic fatty liver (NAFL), osteoporosis, myocardial infarction, ischemia reperfusion injury and aging [22,29,34,40,41,42,43,44,45]. Here, IP6K3 is linked to metabolic disease.