Mice devoid of Akt1 exhibit decreased cell survival observable by growth retardation and decreased in overall organ size and increased perinatal mortality [21, 22]; disruption of Akt2 causes reduction in insulin-stimulated glucose uptake in muscle and fat, so those mice are insulin intolerant and show diabetes-like symptoms [23]; on the other hand Akt3-deficient mice don't display these symptoms but present smaller brain size with a reduced total number of cell as well as decreased average cell size [24]. The gene discussed is INS; the disease is diabetes mellitus.