For instance, the gut commensal Lactobacillus reuteri drove autoimmunity and renal injury in Toll‐like receptor 7 (TLR7)‐dependent lupus model,[34] while interestingly, this microbiota was reported in another disease to regulate the function of ILC3s in the gut.[35] Consequently, it is reasonable to speculate that ILC3s might be involved in the possible causal scenarios behind microbiome interactions with the host in LN progression. This evidence concerns the gene TLR7 and systemic lupus erythematosus.