Mammalian target of rapamycin (mTOR) is highly expressed in various types of hepatocellular carcinoma (HCC). Clinically, HCC cases without inflammation and cirrhosis are also increasingly common, especially in patients with nonalcoholic fatty liver disease, more and more patients develop HCC, which is only characterized by hepatic steatosis. However, the molecular mechanisms underlying the development of non-inflammatory HCC remain unclearly. Our previous study demonstrated that overactivation of mTOR pathway in the liver promotes de novo lipid synthesis and eventually spontaneous formation of non-inflammatory HCC. The continuous activation of mTOR pathway, on the one hand, promotes the de novo synthesis of lipids, resulting in the production of a large amount of lipid in the liver; on the other hand, it inhibits autophagy, resulting in the inability of lipid to be removed in time and accumulate in the liver. Accumulated lipid peroxidation eventually develops into HCC. In addition, the continuously activated mTOR pathway inhibited the release of exosomes by reducing the expression of Rab27A, and in vitro experiments confirmed that hepatoma cells after Rab27A knockout were more prone to invasion and metastasis. The reduced release of exosomes may impair intercellular communication, especially with immune cells, thereby making HCC more prone to invasion and metastasis with less inflammation.