Based on these results, we hypothesize: (1) TGFβ secreted by CRC cells activates TGFβ receptors in tumor cells and increases expression of PDGF-D, (2) secreted PDGF-D subsequently activates PDGFRβ to be overexpressed in tumor cells through autocrine or paracrine mechanisms. This evidence concerns the gene PDGFRB and neoplasm.