H2AX and lung cancer: Consistently, transfection of siKLC4, combined with cisplatin or etoposide, markedly enhanced the accumulation of γ-H2AX at the protein level (Fig. 3d, e, Supplementary Fig. 3b, c), indicating that KLC4 depletion may considerably increase the genotoxic effect of cisplatin and etoposide in aggravating DNA damage in lung cancer cells.