AKT1 and cholangiocarcinoma: The hyperactivation of 5-LO metabolite signaling in CAF-educated MDSC led to the overproduction of the metabolite leukotriene B4 (LTB4), which bound its receptor, leukotriene B4 receptor type 2 (BLT2), to CCA cells, ultimately promoting CCA stemness via the PI3K/Akt/mTOR signaling pathway [136].