A recent study on the function of fibroblasts at different time points after myocardial infarction found that 3 days after myocardial infarction, fibroblasts displayed a proliferative state and promoted angiogenesis through up-regulation of Il4ra signaling, while by 7 days after myocardial infarction, fibroblasts showed an anti-angiogenic homeostatic-like myofibroblast profile and with a step-wise increase in Acta2 expression 35. The gene discussed is ACTA2; the disease is myocardial infarction.