In addition to the EGFR, the insulin-like growth factor-1 receptor (IGF1R) is a major regulator of Akt activation and cross-talk between IGF1R and EGFR or EGFR family members such as Her2 has been reported as a mechanism of resistance against drugs targeting EGFR or Her2 in several types of cancers [16], [23], [24], [25], [26]. Here, AKT1 is linked to cancer.