FSPs are not only tumor-specific neoantigens but also shared by most MSI tumors, as they are the result of certain driver mutations that are positively selected during tumor evolution, e.g., the cMS tract in exon 3 of the TGFBR2 (transforming growth factor beta receptor 2) gene is mutated in around 90% of MSI CRCs [2]. This evidence concerns the gene TGFBR2 and neoplasm.