text: In humans, there are three genes in the Akt family: AKT1, AKT2, and AKT3. These enzymes are members of the serine/threonine-specific protein kinase family ().
  Akt1 is involved in cellular survival pathways and inhibition of apoptotic  processes.  Akt1 is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy, and general tissue growth.   Since it can block apoptosis, and thereby promote cell survival, Akt1 has been implicated as a major factor in many types of cancer. Akt (now also called Akt1) was originally identified as the oncogene in the transforming retrovirus, AKT8.
  Akt2 is important in the insulin signaling pathway. It is required to induce glucose transport.
  These separate roles for Akt1 and Akt2 were demonstrated by studying mice in which either the Akt1 or the Akt2 gene was deleted, or "knocked out".  In a mouse that is null for Akt1 but normal for Akt2, glucose homeostasis is unperturbed, but the animals are smaller, consistent with a role for Akt1 in growth.  In contrast, mice that do not have Akt2 but have normal Akt1 have mild growth deficiency and display a diabetic phenotype (insulin resistance), again consistent with the idea that Akt2 is more specific for the insulin receptor signaling pathway.
  The role of Akt3 is less clear, though it appears to be expressed predominantly in brain. It has been reported that mice lacking Akt3 have small brains.