Altogether, these findings are in agreement with the model in which in MRC5 cells the N exon could be repressed by hnRNP H binding to the GGGG codes, whereas in H69 cancer cells, such repression might be relieved by U2AF65 binding to the N-PU, whose recruiting appears to be facilitated by hnRNP H, leading to N exon activation. Here, U2AF2 is linked to cancer.