HIF1A and neoplasm: Deacetylation at N-terminal lysine residues (K10, K11, K12, K19, and K21) (Geng et al., 2011; Zhang et al., 2017) and acetylation at C-terminal lysine residues (K532, K674, and K709) (Xenaki et al., 2008; Lim et al., 2010; Geng et al., 2012) have been shown to enhance the protein stability of HIF-1α, thus promoting tumor cell tolerance to hypoxic conditions (Geng et al., 2011).