Recent evidence has demonstrated that both short pentraxin, CRP, and long pentraxin, PTX3, modulate inflammation in several cells, including endothelial cells, smooth muscle cells, and fibroblasts [9], [21], [31], Moreover, Nagai et al. recently reported that cardiac-specific overexpression of human CRP induces cardiac remodeling, including de-compensated heart failure and cardiac fibrosis, in response to pressure overload [32]. The gene discussed is CRP; the disease is heart failure.