EMT is regulated by upstream pathways including PI3K/AKT, MAPK, and TGF-β etc.6, 14, 28 Emerging evidence has suggested that EMT is involved in cancer chemoresistance and that inhibiting EMT can reverse this resistance.29, 30 Moreover, EMT has been reported to function in HCC resistance to sorafenib14 and hyperactive PI3K/AKT signaling was one of the primary causes.15, 31 These previous studies indicate that PI3K/AKT signaling hyperactivity may function in Gal-1-induced HCC resistance to sorafenib. This evidence concerns the gene LGALS1 and hepatocellular carcinoma.