The systemic analysis in appropriate leukemic models showed that leukemic cells gain a competitive advantage over normal tissues by developing multiple mechanisms to induces a diabetes-like physio-pathologic condition in the host (impairment of both insulin sensitivity and insulin secretion to provide leukemic cells with increased glucose; induction of high-level production of IGFBP1 from adipose tissue to stimulate insulin sensitivity) and, thus, inducing a subversion of systemic glucose metabolism to allow leukemic progression [260]. The gene discussed is INS; the disease is diabetes mellitus.