Specifically, expression levels of TGIF2 and SMAD7, which restrain TGF‐β induced activation pathways and prevent TGF‐β mediated fibrosis in post‐infarction failing hearts,43 were significantly down‐regulated, while expression of TLR2 and S100A8, which promote inflammation, fibrosis and progression of heart failure,23, 44, 45 were significantly induced in LOY monocytes. The gene discussed is SMAD7; the disease is heart failure.