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. The gene discussed is TRIM63; the disease is diabetes mellitus.