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. This evidence concerns the gene TYK2 and prostate carcinoma.