This was evidenced by the application of combined treatment co-targeting ALK and STAT3 with a new and highly selective STAT3 inhibitor, YHO-1701, that effectively suppressed the adaptive survival of ALK-rearranged lung cancer cells by enhancing apoptosis induction via transcriptional downregulation of the anti-apoptotic factor BCL-XL. The gene discussed is ALK; the disease is lung carcinoma.