More important, the reduction of p-ERK in shIWS1 cells was rescued by U2AF65α, but not by U2AF65β (Fig. 5g, Supplementary Fig. 7f, lower panels), confirming that the activity of the p-IWS1/Sororin/p-ERK axis in lung adenocarcinomas depends on the alternative RNA splicing of U2AF2. This evidence concerns the gene CDCA5 and lung adenocarcinoma.