The crosstalk between CAFs and immune cells stimulates cancer progression and therapeutic resistance.[15] In this study, we found that patients in the high-risk group were significantly associated with a higher expression of immune checkpoint molecules, such as PD-1, PD-L1, and CTLA4 (Fig. 7A–B), which are known to induce T cell dysfunction and predict poor prognosis.[43] Blocking the immune checkpoint proteins via immunotherapy can help activate T cell function. The gene discussed is PDCD1; the disease is cancer.