Likewise, we have identified splice junctions in cancer that deviate from normal tissues in functional domains implicated in cancer signaling, such as PKC-like [33], DEAD-like [54] and RING [55] domains, in genes associated with cancer, such as CSNK2A1, CSNK2A2, RIOK1, PRKDC, TYK2, PAK1, and IRAK1, for which gene expression and posttranslational modifications act as mechanisms for cancer progression [56–61]. The gene discussed is PAK1; the disease is cancer.