FSTL3 can act as a bridging molecule for the crosstalk between HIPPO/YAP1 and Wnt/β-catenin pathways. Activation of YAP1 induces FSTL3 expression, which in turn activates the β-catenin pathway. β-catenin can induce YAP1, which trans-activates FSTL3, thereby forming a positive feedback loop and promoting EMT, aerobic glycolysis, invasion and metastasis of colorectal cancer cells. In addition, FSTL3 is associated with chemoresistance in lymph node metastasis and can be used as a marker of poor prognosis. This evidence concerns the gene FSTL3 and colorectal cancer.