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. Here, HIF1A is linked to neoplasm.