Furthermore, the tolerance and suppression of anti-tumor immune response via abnormal expression of immune checkpoint such as PD-1/PD-L1 in tumor immune microenvironment (TME) largely contributes the tumor immune escape [31].TRIM16 influenced the expression of PD-L1 by regulating the JAK/STAT signaling pathway in non-small cell lung cancer, and TRIM28 was related to the resistance of cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) blockade by the ubiquitination of AMP-activated protein kinase in melanoma [32, 33]. The gene discussed is SOAT1; the disease is neoplasm.