Small molecules that inhibit splicing have antitumor activity [15, 16]; the SF3b component PHF5A is differentially required for constitutive splicing in glioblastoma versus normal neural stem cells [17]; RNA splicing is reportedly noisier in cancers than normal cells [18]; increased intron retention is associated with SETD2 mutations in kidney cancer [19] and castration resistance in prostate cancer [20]. This evidence concerns the gene SETD2 and cancer.