Recent studies showed that inflammation increases PD‐L1 expression through CSN5, which reduces PD‐L1 ubiquitination and leads to its stabilization.13 CSN5 was identified as a PD‐L1‐interacting partner using MS analysis, confirming an association between PD‐L1 and CSN5 in breast cancer.13 We also determined the function of CSN5, USP15, and CSN8 in our system and found that they did not affect PD‐L1 protein expression and stability. This evidence concerns the gene COPS5 and breast carcinoma.