Additionally, IGF2BP1 loss enhanced the levels of HGF, which is produced by stromal fibroblasts and contributes to epithelial cell proliferation and invasive growth of CRC cells by the interaction with β-catenin signaling, and conferred resistance to EGFR inhibitors in colon tumor-initiating cells in fibroblasts in vitro, and increased fibroblast cell growth [16, 71–74], indicating a potentially tumor-suppressive role of IGF2BP1 via modulating HGF in fibroblasts. Here, HGF is linked to neoplasm.