CD44 and cancer: The following evidence supports this assumption: (i) abundant differential AS events, instead of a small number of DEGs, are strongly influenced upon MEN1 knockout in mouse lung tissue and human cancer cells; (ii) menin extensively binds to CD44 variant exons and reduces their abundance by slowing Pol II elongation; and (iii) in MEN1-regulated SE events, RNA splicing isoform levels, rather than their corresponding transcription levels, correlate with LUAD patient survival (Figure 5J; Supplementary Figure S5J).