Future studies are warranted to systematically assess the potential of FTO for HF prevention and treatment.274 For cardiac fibrosis, METTL3 could repress androgen receptor (AR) expression in a YTHDF2-dependent manner, which activates HIF-1α signaling, thus enhancing glycolysis and cardiac fibroblast proliferation.275 Cai et al. revealed the potential metabolic-related regulation of RNA modification in osteogenic differentiation, inspiring future clinical applications in metabolic bone diseases and stem cell therapy. The gene discussed is FTO; the disease is hydrops fetalis.