MTOR and neoplasm: FABP1 is significantly upregulated in some HCCs, promoting tumour growth, angiogenesis, and metastasis through VEGF-A transcription (via Akt/mTOR–HIF1α) and downstream signalling through VEGFR2 in cholesterol-rich domains. Other studies show downregulation of FABP1 in HCCs, associated with poor survival and reduced lipid accumulation. Overexpression inhibits proliferation, migration, and invasion, and promotes apoptosis.