Deng et al[43] indicated that druggable alterations in RTKs were present in 37% of all patients with GC, and FGFR2 was the RTK that was amplified the most often (9.3%), followed by KRAS (8.8%), EGFR (7.7%), and ERBB2 (7.2%).[43] According to Cox multivariate analysis, the EGFR amplification status independently functioned as an indicator of unfavourable prognosis in patients with GC, which was independent of chromosomal instability.[43]. This evidence concerns the gene ERBB2 and gastric cancer.