Catecholamine hypersecretion, also known as pheochromocytoma, originates in the adrenal medulla, sympathetic ganglion, parasympathetic ganglion (paraganglia) or other sites of chromophobic tissue. Due to the paroxysmal or persistent secretion of norepinephrine and epinephrine by the tumor cells, the clinical picture is one of paroxysmal or persistent hypertension, headache, sweating, palpitations and metabolic disorders. Pheochromocytoma can be cured if treated early. Pheochromocytomas located in the adrenal glands account for 80% to 90% of cases and are mostly one-sided; extra-adrenal tumors are mainly located in the extra-peritoneal area and parietal aorta (10% to 15%), and a few are located in special areas such as the hilum, hepatic hilum, bladder and retrorectum. Most of them are benign and 10% are malignant. As with most tumors, the etiology of disseminated pheochromocytoma remains unclear. Familial pheochromocytomas, on the other hand, are genetically related. Pheochromocytomas in multiple endocrine adenomatosis (MEN-2A, MEN-2B) have been reported to have a deletion of the short arm of chromosome 1, and both have been found to have germ-line mutations in the REI proto-oncogene on chromosome 10, with MEN2A showing a mutation in exon 10 of RET, which encodes a cysteine residue in the ligand-binding region of the extracellular protein cysteine residues that affect the tyrosine kinase receptor on the cell surface, while MEN-2B has a mutation in the RETB proto-oncogene on chromosome 10, which affects the tyrosine kinase catalytic site in the intracellular protein binding region. Tyrosine kinases are implicated in the regulation of cell growth and metamorphosis. This leads to the development of disease in susceptible individuals. In pheochromocytoma in vonHippel-Lindau syndrome, genetic damage is present in the VHL gene (also known as tumor suppressor gene) at 3p25-26, with a variety of mutations, which can occur in all three exons (exons 1, 2, and 3) and can be expressed as nonsense mutations, missense mutations, shift mutations, or deletion mutations. Mutations in the germ cell line of the VHL gene determine the susceptibility and development of tumors in VHL families, while mutations in the somatic cell line of the VHL gene are associated with the malignant tendency of the tumors that occur. In multiple neurofibromas (types I and II), pheochromocytoma is only associated with type I. The underlying genetic damage is an inactivating mutation in the RFl gene on chromosome 17. This gene is also a tumor suppressor gene, and its loss of expression can lead to the development of pheochromocytoma and other tumors.