It has been found that IRSp53 is tyrosine phosphorylated at multiple sites in response to EGFR stimulation, and knocking down of IRSp53 diminished cell proliferation in cells that v-Src transformed and tumor formation in mice through p-AKT/p-Stat3/cyclin D1 signaling pathway (Figure 3A) [7, 8]. This evidence concerns the gene AKT1 and neoplasm.