Gastric cancer can be divided in four molecular subtypes (based on TCGA molecular classification): Epstein–Barr virus (EBV) tumors (characterized by PIK3CA mutations, PD-L1/2 and JAK2 amplifications, and extensive CpG island methylation); MSI tumors with hypermutation and MLH1 silencing; genomically stable tumors enriched in diffuse histology and carrying RHOA mutations or CLDN18–ARHGAP fusions; and chromosomal instability (CIN) tumors (characterized by aneuploidy, frequent TP53 mutations, and amplifications of receptor tyrosine kinases such as ERBB2, EGFR, and MET) [60]. This evidence concerns the gene EGFR and gastric cancer.