timp1−/−, timp2−/− and timp4−/− mice display apparently normal phenotypes but exhibit interesting features associated with the absence of TIMPs, such as impaired learning due to abnormal neural plasticity in timp1−/− mice [229], no proMMP2 activation in timp2−/− mice [230], and increased mortality after myocardial infarction induction in timp4−/− mice [231]. The gene discussed is TIMP2; the disease is myocardial infarction.