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. The gene discussed is PTPN11; the disease is colorectal carcinoma.