To further explore whether TREX1 overexpression could induce chemoresistance by itself or additional mechanisms are involved, we next stably transduced DMS114 cells (originally derived from a patient with chemonaïve SCLC) and H82 (derived from a patient previously treated with chemotherapy) with TREX1-WT or TREX1 mutant constructs and evaluated cisplatin and etoposide effects on cell viability. Here, TREX1 is linked to small cell lung carcinoma.