Notably, several studies have linked the IFNγ signature to IFNG expression, specific clinical features, SLE disease activity index (SLEDAI), dsDNA levels, substantial tissue damage particularly in proliferative LN, and inversely correlated with complement (C3 and C4) levels, warranting further investigation into its clinical implications [3, 42]. This evidence concerns the gene IFNG and systemic lupus erythematosus.