However, when stressed by myocardial infarction, Fbln2-null mice develop a phenotype of reduced cardiac tissue remodeling, attenuated TGF-β signaling within damaged cardiac tissues, and significantly improved survival [9], implying that fibulin-2 is required for repair of tissues damaged by hypoxic stress, a known driver of malignant progression of epithelial tumors [9]. The gene discussed is FBLN2; the disease is myocardial infarction.