Axitinib treatment resulted in an increased percentage of cells undergoing necrotic-like death (Annexin V−/PI+) and secondary necrosis (Annexin V+/PI+) upon drug exposure in both RCC cell lines, being the frequency of dead cells higher and the cell death program more advanced in A-498 cells as compared to Caki-2 cells (Figure 6C); moreover, neither DNA fragmentation (Figure 6D) or caspase-3 activation (Figure 6E) was evidenced in axitinib-treated RCC cells. This evidence concerns the gene CASP3 and renal cell carcinoma.