However, KRAS or BRAF gain-of-function mutations are frequently observed in multiple cancer types, especially in CRC, pancreatic cancer, and non-small-cell lung cancers (NSCLC) (Network, 2012; Zehir et al., 2017), which may hijack the function of SHP2 as the key mediator of multiple RTKs to control the ERK and AKT signaling. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.