Loss of the ATPase and RNA helicase activity of DDX39B caused by E197A or SAT/AAA mutant35 also triggered the phosphorylation and ubiquitination of ECAD, accompanied by decreased ECAD protein level in NSCLC cells, suggesting that DDX39B-induced ECAD degradation was independent of its unwinding activity (Supplementary Fig. 8a, b). The gene discussed is CDH1; the disease is non-small cell lung carcinoma.