Given the growing evidence that PPARs have anti-inflammatory activity by competitively inhibiting NF-κB and AP1 (cJun/cFos) experimentally (recently reviewed by Lockyer et al. [80]), it is possible that reduced (or ablated) MuRF2 in patients may increase their susceptibility to infection in addition to diabetes as we demonstrate in the present study. This evidence concerns the gene TRIM55 and infection.