Overexpressed protein tyrosine phosphatase N2 (PTPN2) renders tumor resistant to immunotherapy by negatively regulating IFN‐γ signaling with JAK/STAT pathway.[9] On the one hand, downregulating PD‐L1‐positive cells via CRISPR/Cas9 can revive the slumbering T cells and elicit T cell‐mediated adaptive immunity.[10] On the other hand, deficiency of PTPN2 can improve recognition of tumor cells and susceptibility to cytotoxic CD8+ T cells by invoking an IFN‐γ response. This evidence concerns the gene SOAT1 and neoplasm.