Knockout of methyltransferase-like 3 (Mettl3) leads to a decrease in bone mass in mice, a decrease in osteogenic potential and increased adipogenic differentiation of BMSCs, and accumulation of adipose tissue in the bone marrow, while overexpression of Mettl3 protects mice from osteoporosis caused by estrogen deficiency [103]. This evidence concerns the gene METTL3 and osteoporosis.