In gastric cancer (GC), despite a low-frequency of genomic alterations [55,56], routine tissue-based NGS showed that at least 37% of patients harbor somatic mutations (TP53, KRAS) or gene amplification, such as HER2, MET, EGFR, and FGFR2 [57,58,59,60]. Here, KRAS is linked to gastric cancer.