Simultaneous administration with MS-444 completely abolished this pro-tumoral phenotype and reactivated local immune response, which critically underlined the importance of HuR in modulation of tumor immunity and implicated endogenous HuR as a valuable measure to predict the clinical response to PD-1-PD-L1-based immunotherapies, and more importantly, as an alternative target to CMTM6 for indirect interference of PD-L1 expression in tumor. This evidence concerns the gene CD274 and neoplasm.