In addition, the recent immunolocalization of GPER in testicular tumors and the reports indicating that GPER activation by selective ligands can allow for opposite outcomes in different testicular cells (i.e., seminoma and Leydig cells) (Figure 1) should open new perspectives to define the mechanisms behind the development of estrogen-dependent testicular tumorigenesis as well as to provide a new target for the development of new pharmacological tools against testicular cancer. Here, GPER1 is linked to testicular cancer.