CCNA2 and gastric cancer: 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.