TRIM8 is a ubiquitin E3 ligase that promoting TAK1 Lys63-ubiquitination (NF-κB) and relieving STAT inhibition via PIAS3 degradation (JAK/STAT) [5, 22], so elevated TRIM8 in active LN is biologically credible, but TRIM8 dysregulation can also occur in other autoimmune conditions such as OA and keratitis [23, 24] and non-autoimmune glomerulonephritis [25]. This evidence concerns the gene NFKB1 and autoimmune glomerulonephritis.