The different mechanisms through which testosterone causes polycythemia include stimulating erythropoietin production and decreasing hepcidin production, promoting erythropoiesis, and increasing iron availability [4]. While venous thromboembolic events such as deep vein thrombosis (DVT) and pulmonary embolism (PE) are more frequently reported, testosterone-associated CVST is underrecognized [1]. This case highlights the importance of recognizing CVST as a potential complication of secondary polycythemia due to testosterone use, as well as its management. The gene discussed is HAMP; the disease is deep vein thrombosis.