Interestingly, analysis of the single isoforms revealed that IRF5 variants originating from alternative splicing (V2 and V3) and missing the first 48 nucleotides of the PEST domain-encoding region are resistant to TRIM21-mediated degradation and inhibition, thus suggesting that the enhanced expression of these isoforms in SLE patient monocytes may be as a result of decreased ability of TRIM21 to degrade them [23]. Here, IRF5 is linked to systemic lupus erythematosus.