MYD88 and systemic lupus erythematosus: It is noteworthy that, Zarate-Neira et al. 27 found that mouse miR-200a-3p expression was significantly increased in a systemic lupus erythematosus (SLE) model and can inhibit the TLR4/MyD88 signalling pathway and promote interferon production, thereby regulating the immune response in mice and proving its usefulness as a biomarker of SLE.