In a mouse SLE model with a homozygous Faslpr mutation, exosomes were used to supply Fas-impaired cells with Fas protein so as to reduce intracellular miR-29b levels; this prevented Dnmt1-mediated hypermethylation of Notch1 promoter and maintained the ability of MSCs to differentiate into osteoblasts. The gene discussed is FAS; the disease is systemic lupus erythematosus.