Therefore, our results suggest that an increase in CMTM3 leads to an increase in cancer-associated cells such as fibroblasts, macrophages, myeloid dendritic cells, and endothelial cells, which can potentially modulate the protumor immune microenvironment, thereby helping tumors achieving immune escape, which ultimately is not conducive to improving the effectiveness of tumor immunotherapy. This evidence concerns the gene CMTM3 and neoplasm.