Together, these data indicate that, whereas MK2 and XPA inhibition alone sensitizes established refractory lung adenocarcinoma tumors to cisplatin, (with MK2 inhibition being superior to that of XPA inhibition alone, based on residual tumor burden), co-targeting of XPA and MK2 within the same tumor further reduces tumor burden with a notably increased efficiency (Fig. 4c–e; Supplementary Fig. 8A, B). This evidence concerns the gene XPA and neoplasm.