METTL3 and Down syndrome: Shi et al. (2021) considered that METTL3 preserved mitochondrial function in Down syndrome by reducing the expression of nuclear receptor-interacting protein 1 (NRIP1), a crucial gene in the regulation of the mitochondrial pathway. But Zhang et al. (2021) demonstrated that METTL3 and YTHDF2 cooperatively promoted mitochondrial dysfunction and inflammatory response during oxLDL-induced inflammation in monocytes. In addition, the demethylase FTO inhibitor MO-I-500 was found to ameliorate astrocyte mitochondrial dysfunction in streptozotocin-induced AD cell models (Cockova et al., 2021).