In prostate cancer, SPOP mutations occur in approximately 10% of patients, where it acts as a tumor suppressor by degrading oncogenic transcription factors, including ERG (5, 6), DEK (3), and TRIM24 (3), and by mediating poly(ADP-ribose) polymerase inhibitor–induced tumor suppression via stimulator of interferon gene (STING) stabilization (18). Here, STING1 is linked to neoplasm.