In order to understand how malfunction of a single member of the TGF-ß signaling pathway, the TGFBR2, alters the cellular proteomic and glycomic landscape in MSI colorectal cancer cells, we previously established a MSI cell line model system that enables doxycycline (Dox)-regulated reconstitution of TGFBR2 expression and signal transduction in an isogenic background [13]. This evidence concerns the gene TGFBR2 and colorectal cancer.