The significance of miR-146a in SLE pathogenesis is further supported by studies demonstrating that miR-146a-deficient mice develop an SLE-like phenotype, characterized by hyperresponsive T cells, increased expression of activation markers such as CD69 and CD44, and enhanced cytokine production, including IFN-γ and IL-17. This evidence concerns the gene IFNG and systemic lupus erythematosus.