By evaluating a large number of target genes that were mutated at variable rates in their coding repeat sequences, we show a significant decay of the corresponding mutant mRNAs compared to wild-type in MSI primary CRCs with a significant impact of endogenous expression of UPF1 in this process, with UPF2 playing a minor role in the process, as recently described by our group in a series of MSI CRC cell lines [14]. The gene discussed is UPF1; the disease is colorectal carcinoma.