Direct mechanisms include the induction of endoplasmic reticulum stress leading to caspase-mediated apoptosis, upregulation of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) expression promoting cell death, inhibition of angiogenesis via downregulation of growth factors such as bFGF causing tumour hypoxia and central necrosis, and enhanced tumour antigen presentation through increased major histocompatibility complex class 1 (MHC-I) expression [11]. This evidence concerns the gene FGF2 and neoplasm.