A recent whole-exome and transcriptome comprehensive study including 31 cancer types identified 14,438 splicing-associated variants, most of which were shown to disrupt donor and acceptor sites and to cause exon skipping, intron retention and alternative 5′ or 3′ splicing site usage particularly in TP53 and GATA3 genes (Shiraishi et al., 2018). The gene discussed is TP53; the disease is cancer.