Specifically, Xie et al. analyzed immunohistochemistry and RNA-sequencing data for patients with HCC and demonstrated that high expression of OX40 regulated the activation of T cells, expansion of suppressive Tregs and upregulation of Tim-3 expression as well as CD8A, CD68, LAG3, and PD-1 expression [91], which provided a rationale for reversing multiple immunosuppressive pathways via therapeutic targeting of OX40 and blocking associated immune checkpoints in HCC patients. Here, CD68 is linked to hepatocellular carcinoma.