In addition, while depletion of mutant KRAS reversed cytotoxicity to BI-2536 and volasertib (Figure 4d), co-expression of CCNA2 in this context was sufficient to reintroduce sensitivity (Figure 4e), indicating that sensitivity to PLK1 inhibitors in KRAS mutant gastric cancer cells is mediated by CCNA2 upregulation. This evidence concerns the gene KRAS and gastric cancer.