Of note, in the lung adenocarcinoma cells in which XPA was knocked down, we observed elevated levels of γH2AX, phospho-p38, phospho-MK2, and phospho-Chk1 even in the absence of cisplatin treatment, consistent with elevated basal levels of endogenous DNA damage in tumor cells compared to non-tumorigenic fibroblasts (Fig. 1d)33,34. Here, XPA is linked to lung adenocarcinoma.