The exact mechanisms of cytotoxic action of splicing inhibitors on cellular processes are still poorly understood, but the main consequences of spliceosome blockade can be noted: unproductive splicing and subsequent nonsense-mediated decay of DNA repair transcripts (CHEK2) [171] or the generation of pro-apoptotic protein isoforms (Mcl-1S) [172]; a large number of transcripts with retained introns forming an excess of double-stranded RNA in cytoplasm with the following activation of antiviral signaling and apoptosis of cancer cells [173]. The gene discussed is CHEK2; the disease is cancer.