AKT1 and breast carcinoma: Noteworthy is the fact that the expression of AKT isoforms fused to an N-terminal Src myristylation signal (MGAG residues), which allows Akt to associate with the plasma membrane via a mechanism that precludes the PH domain, is enough to transform embryonic fibroblasts and increase the development of mammary carcinoma when expressed in a transgenic mouse model via the mammary-specific mouse mammary tumor virus (MMTV) promoter [75–77].