Considering what is known concerning the activity of these intermediates and the data shown here, we propose a model for GRPR signaling under an ETS-rearrangement cellular context (Fig. 5), where TYK2, MST1 and p-Akt may constitute promising therapeutic targets that should be explored in combination with GRPR inhibitors for treating these particular subtypes of prostate cancer. The gene discussed is TYK2; the disease is Familial prostate cancer.