This combined effort for the first time permitted to use the complete information gathered by the human genome sequencing projects to systematically delineate potential candidate genes that may be mutated during MSI-driven carcinogenesis. We have determined the mutation frequency of particularly long coding and untranslated MNRs. Based on all available MNR mutation information we established a statistical model for the prediction of selective MSI target genes in an organ specific manner. Experimental analysis of predicted target genes in colorectal cancer extended to colorectal adenomas revealed that these genetic alterations are not restricted to carcinomas but already occurred early during tumorigenesis. We now seek to translate these findings to shorter coding MNRs. Finally, we will extend these analyses to the genome of other species with emphasis on the mouse, in order to identify common or different coding microsatellite target genes contributing to the MSI tumor pathway.