In NSCLC, Ota et al. reported that forced expression of echinoderm microtubule-associated protein-4 (EML4)-ALK oncoprotein in Ba/F3 cells increased PD-L1 expression, whereas endogenous PD-L1 expression in EML4-ALK-positive NSCLC cells was attenuated by the ALK inhibitor alectinib and by siRNA-mediated ALK knockdown [91]. This evidence concerns the gene EML4 and non-small cell lung carcinoma.