Liu et al., demonstrated that increased let-7a/e/i/g in kidney tissue samples of lupus nephritis (LN) patients could modulate the activation of NF-κB by targeting TNFAIP3, besides, lin28, a negative regulator of let-7 miRNAs, was found to be decreased in kidney samples from LN patients compared to the control samples, these results indicate a Lin28-Let-7-TNFAIP3 axis during the pathogenesis of LN (25), but none of these let-7 studies focusing on the bone marrow microenvironment in lupus pathogenesis, especially BM-MSCs. Here, NFKB1 is linked to lobular neoplasia.