Indeed, when comparing pathway activities (Fig. 3E), TGFβ was active in all HF models, however, strongest activity was found in AngII and late MI models while in early MI fibroblasts proinflammatory TNFα, NFκB, as well as hypoxia, and JAK-STAT pathways were induced. The gene discussed is SOAT1; the disease is myocardial infarction.