Given that thepredominant U2AF65 isoform in high p-IWS1 tumors is the U2AF65α isoform, whichbinds Prp19, while the predominant isoform in the low p-IWS1 tumors is U2AF65β,which does not interact with Prp19, these data indicate that in lungadenocarcinoma patients, as in cultured tumor cells, the recruitment of Prp19 tothe CAR-Elements is mediated by U2AF65. This evidence concerns the gene PRPF19 and neoplasm.