The results showed that (i) most tumors had significantly higher level of SIRPG expression than matched normal tissues and high SIRPG expression correlated with a “hot” tumor immune phenotype; (ii) high SIRPG expression was associated with markedly better response to PD-1 blockade in both NSCLC and melanoma; (iii) SIRPG expression in T cells facilitated expression of several immune checkpoint molecules (e.g., PDCD1 and CTLA4), resulting in the transition of T cell’s phenotype and cytotoxicity. This evidence concerns the gene CTLA4 and neoplasm.