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. The gene discussed is TLR7; the disease is lobular neoplasia.