In organ‐specific manifestations, A20 deficiency in podocytes exacerbates lupus nephritis by dysregulating the NF‐κB/UCH‐L1 axis, while rare de novo mutations have been shown to impair A20's ubiquitin‐editing of TRAF6, potentially compromising the blood‐brain barrier in neuropsychiatric SLE [328]. Here, TNFAIP3 is linked to lupus nephritis.