Some of the above questions may be answered after identification of the specific molecular changes responsible for pheochromocytoma and the mechanisms linking identified germline or somatic genetic alterations to expression of specific tumor-cell phenotypes and clinical features of disease. New techniques, such as complementary DNA microarray analysis and laser-capture microdissection, offer tremendous potential for tracing phenotypic differences in tumors to underlying differences in gene expression and ultimately to the mutations responsible for the tumor. Such findings may lead to improved understanding of mechanisms of tumorigenesis, variations in the rate of disease progression, metastatic potential, tendency to recurrence, metabolic and hemodynamic alterations, variations in sensitivity and specificity of diagnostic tests, and development of and predicted responsiveness to novel treatments. For example, knowledge about expression of specific antigens or proteins, such as membrane catecholamine transporters, could lead to improvements in tumor imaging methods. It could also facilitate novel “magic bullet” therapy by targeting radionuclides, cytotoxins, or vaccines to tumor cells. This may be important, not only for treatment of malignant pheochromocytoma but also for prevention of pheochromocytoma in at-risk patients.