AKT1 and intrahepatic cholangiocarcinoma: In a study of α6β1 and α6β4, Ding et al. reported that α6 overexpression was significantly correlated with larger tumors, multiple nodules, microvascular/bile duct invasion, and lymphatic metastasis, and an lower OS rate in ICC patients; they indicated that high α6 expression enhanced the activation of extracellular signal-regulated kinases (ERK1/2) and protein kinase B (AKT) signals, inducing ICC cell metastasis and invasion [14].