Mechanistically, we identified p-STAT3 and its downstream targets MMP-2 and MMP-9 as mediators of the protumorigenic function of SLCO1B3. The STAT3 signaling is overactivated in the CRC, and its downstream mediators such as VEGF, c-Myc and Cyclin D1, MMP-2, and MMP-9 have been linked with tumor angiogenesis, proliferation, invasion, and metastasis, respectively [17–19]. This evidence concerns the gene STAT3 and neoplasm.