In addition, we also found that AFE exhibited antioxidant activity by activating Nrf2 expression in CRC cells (Figure S1), but it elicited anticancer activity through regulation of PI3K/AKT, MAPK, Wnt/β-catenin, JAK2/Stat3, and NFκB/IL-6/Stat3 signal transductions in CT26 cells, which was consistent with what we observed in the AOM/DSS-induced CAC mice. The gene discussed is STAT3; the disease is colorectal carcinoma.