HIF1A and neoplasm: A mouse model harboring a lysine-to-alanine substitution at HIF-1α Lys32, which prevents its monomethylation, exhibited much higher HIF-1α levels, upregulated hypoxia-inducible gene expression, as well as enhanced tumor growth and angiogenesis [14], suggesting that monomethylation at this lysine residue is a critical regulator of HIF-1α function.