It was observed as a cisplatin resistance factor in ovarian cancer cell lines, which cannot be interpreted as a function of the CLPTM1L gene during oncogenesis.9,14 A recent study demonstrated that CLPTM1L, as an over expressed protein in lung tumor cells, protected cells from genotoxic stress induced apoptosis through regulation of Bcl-xL, which implicated an anti-apoptotic CLPTM1L function as a potential mechanism of susceptibility to lung tumorigenesis.15 This evidence concerns the gene BCL2L1 and ovarian cancer.