Since TLR4 downregulation was identified as an anti-inflammatory mechanism of the insulin-sensitizer incretin glucagon-like peptide-1 (GLP-1) [122], and considering that a PPARβ/δ agonist markedly upregulated GLP-1 in obese T2DM mice [123], it is possible that PPARβ/δ stimulation may be a valid therapeutic tool for DCM. The gene discussed is GCG; the disease is familial dilated cardiomyopathy.