Alpha-fetoprotein (AFP), human choriogonadotropin (hCG) and lactate dehydrogenase (LDH) are established tumour markers of testicular germ cell tumours (TGCT) which are used according to the guidelines for primary diagnosis, staging, monitoring of therapeutic response and follow-up. Placental alkaline phosphatase and neurone-specific enolase play no role at all in the diagnosis and management of TGCT.Metastasized TGCT are classified according to the IGCCCG classification system into tumours with good, intermediate and poor prognosis depending on their serum concentration. The risk classification has a direct impact on therapy and determines the intensity of chemotherapy. In rare cases AFP and hCG might be elevated due to non-testicular reasons which have to be taken into consideration for the differential diagnosis especially if marker concentration and clinical presentation do not match. Response to chemotherapy is monitored with AFP and hCG which are determined the day before initiation of the next treatment cycle. Marker increases during or shortly after discontinuation of chemotherapy indicate a poor prognosis and make the immediate initiation of salvage treatment regimes necessary. Only 40-50% and 30% of relapses in patients under active surveillance for clinical stage I disease and after systemic chemotherapy are associated with marker increases. The remainder will be diagnosed by imaging studies or clinical symptoms. Marker increases have to be validated by imaging studies. However, about 10% of all relapsing patients have marker increases only without any imaging evidence of metastatic disease. Residual masses of any size and location have to be treated by postchemotherapy resection once the marker concentration is normalized or once it has reached a stable plateau. So-called desperation surgery in the presence of rising tumour markers is only indicated if no curative chemotherapy is available, all residual masses are completely resectable and no hCG elevation are observed. For follow-up, AFP, hCG and LDH should be evaluated for advanced TGCT and clinical stage I nonseminomas, whereas clinical stage I seminomas should be monitored without any markers.