Much remains to be learned about how PDE11A loss-of-function mutations contribute to the molecular mechanisms of NSGCT pathogenesis (i.e., do PDE11A mutations work primarily in Leydig and/or Sertoli cells, and thereby alter the testicular hormone environment, or do they act directly on germ cell precursors, or both)? The gene discussed is PDE11A; the disease is nongerminomatous germ cell tumor.