The depletion of METTL3 was shown topromote cell differentiation and reduce cell proliferation in humanhematopoietic stem/progenitor cells (HSPCs) [24].Conditional knockout of METTL3 in MSCs inducedpathological phenotypes of osteoporosis and brought about damaged boneformation, enhanced adipogenic capacity, together with incompetent osteogenicdifferentiation potential in [25].Meanwhile, METTL3 participates in the regulation of the PI3K-AKT signalingpathway too. Here, METTL3 is linked to osteoporosis.