Closer analysis of the peri‐infarct border showed that dual treatment of VEGF/IGFBP‐4 resulted in significant and synergistic decreases in the expressions of fibrosis markers collagen I and collagen III following MI (Figure 1C), which can be attributed to the enhanced angiogenic action of VEGF, but only when the ischaemic myocardium is not too damaged beyond repair such as following IGFBP‐4 treatment. The gene discussed is IGFBP4; the disease is myocardial infarction.