In addition to 1q gains, further the chromosome 2q gains (found in CNA-PC52) that we find associated with NMD efficiency are interesting to follow-up, since this arm encompasses candidate genes CWC22 and SF3B1 implicated in the splicing process, whose dysregulation may plausibly affect NMD. It was shown that mutations in the spliceosome genes SF3B1 and U2AF1 render cancer cells more sensitive to NMD inhibition in a synthetic lethality fashion [30, 107, 108] adding confidence that CNA of this same gene might disbalance NMD. This evidence concerns the gene U2AF1 and cancer.