From a mechanistic point of view, it was shown that cholesterol binds to the ER-anchored FAF2 protein, which allows the formation of the SNHG6–FAF2–mTOR complex, through which the SNHG6 co-ordinates the mTORC1 kinase cascade activation and cellular cholesterol biosynthesis in a self-amplified cycle that speeds up the cholesterol-driven NAFLD to HCC transition. Here, FAF2 is linked to metabolic dysfunction-associated steatotic liver disease.