The work ahead necessary to develop and refine clinically useful antiapoptotic therapy in ischemic-reperfusion injury is daunting. There are many unanswered questions. What is the best method of detecting apoptosis in the cardiac myocytes? What will be the most practical method to deliver this therapy to the cardiac myocyte? Will antiapoptotic agents act selectively on affected myocytes to provide clinical efficacy? Will antiapoptotic agents be effective, or will they be limited by dose heterogeneity? If antiapoptotic is proven to have long lasting efficacy, should it be used for all patients with myocardial infarction or confined only to patients with left ventricular dysfunction. Will antiapoptotic therapy be so effective that it replaces ACE inhibitors and betablockers, or will it always be used as an adjunct to an ACE inhibitor or a betablocker? These questions lay the foundation for investigation for the next decade.