PIK3CA and neoplasm: Additional activating mutations in CRC driver genes/pathways may also “crosstalk” (e.g., HGF, PI3K/AKT, TNKS2) with Wnt signaling to facilitate rapid proliferation into a fully malignant tumor (via β-catenin stabilization, nuclear translocation, and cotransactivation of TEF/LEF-occupied gene promoters).