revealed that SPOP inhibited the immune escape of cancer cells by degrading PD‐L1 in prostate cancer.[32] In this study, we demonstrated that SRC‐1 could interact with SPOP but could not be degraded by SPOP, suggesting that SRC‐1 executes a sponge‐like function to absorb SPOP, leading to reduce the chances of the interaction between SPOP and PD‐L1, and consequently stabilize PD‐L1. The gene discussed is NCOA1; the disease is prostate carcinoma.