Specifically, the hypoxic environment promotes upregulation of METTL14/ALKBH5 [166, 234] and subsequently modulates m6A levels of EMT and angiogenesis-related transcripts (including genes involved in transforming growth factor-β signaling), leading to inappropriate cell cycle progression and tumor evasion of apoptosis [194]. The gene discussed is ALKBH5; the disease is neoplasm.