In our study, AFE restrained the activation of JNK and p-ERK and downregulated the level of its downstream target gene c-fos, probably implying that AFE suppressed the inflammatory response, reduced colon injury, and impeded CRC development via NF-κB/IL-6/Stat3, JAK2/Stat3, and MAPK signal transductions. The gene discussed is STAT3; the disease is colorectal carcinoma.