Our conclusion is based upon the following lines of evidence: (1) Ectopically expressed or endogenous RPS27L interacts with endogenous FANCD2 and FANCI (Fig. 1); (2) RPS27L knockdown via lenti-viral or siRNA approach specifically reduces the levels of FANCD2 and FANCI in the absence and presence of MMC (Fig. 2); (3) RPS27L knockdown impairs the formation of FANCD2 foci and decreases ICL repair efficiency upon MMC treatment (Fig. 4A, C); (4) RPS27L knockdown inhibits cell viability and colony formation after MMC treatment in lung cancer cells (Fig. 4D, E). The gene discussed is RPS27L; the disease is lung cancer.