In the early 1990s, this conceptual framework on an intracellular localization and action of insulin was expanded by a novel proposal according to which insulin may physically interact with the (mainly nuclear) retinoblastoma tumor suppressor protein (RB) and thereby, similar to RB-binding viral oncoproteins, inactivate RB and thus promote cell proliferation [9] which was subsequently validated experimentally [10-13], primarily in human tumor cell culture models [11-13]. The gene discussed is INS; the disease is neoplasm.