This conclusion is supported by several lines evidence: increased expression of miR-128-3p and decreased expression of SPTAN1 in lung cancer cells treated with MMC; a putative SPTAN1 binding site in the 3′-UTR that is subject to miR-128-3p regulation; overexpression of miR-128-3p augmented MMC-mediated chromosomal instability and cell cycle arrest of G2/M phase in lung cancer cells; these biological dysfunctions were caused by disruption of the αII Sp/FANCA/XPF complex induced by miR-128-3p. The gene discussed is ERCC4; the disease is lung carcinoma.