Notably, overexpression of a constitutively active mutant of either AKT2 (myristoylated AKT2) or Src (GFP-tagged Src/Y527F) in Neu cells did not significantly enhance cell proliferation but completely abolished PTx-inhibited cell growth (Supplemental Figure 6, A and B), suggesting that Gi/o-GPCR signaling promotes breast cancer cell growth, at least in part, through the redundant function of the AKT and Src pathways. This evidence concerns the gene AKT1 and breast carcinoma.