Recent studies revealed that phosphatases had a controversial in antitumor immune response: PTEN induced a tumor-intrinsic T-cell-inflamed state resulting in response to ICIs42 and SOCS2 impaired the dendritic cell-based priming of T cells and limited adaptive antitumor immunity.43 Here, we uncovered that tumor intrinsic PTPN1 and SOCS3 could promote antitumor immunity through restrain the activity of JAK-STAT pathway. The gene discussed is PTPN1; the disease is neoplasm.