AKT activation has been widely reported in HCC and served as an important means for the construction of mouse primary liver cancer models.[28] Activated AKT phosphorylates PCK1 and then activates SREBP2 for cholesterol synthesis.[29] Our findings further reveal cholesterol, upstream of AKT, regulates AKT phosphorylation to promote HCC progression. The gene discussed is PCK1; the disease is liver cancer.