Cancer immunosurveillance is the process by which the immune system recognizes and eliminates cancer cells. However, cancer cells can avoid this process through immunoselection (selection of non-immunogenic variants) and immunosupversion (suppression of immune responses). The immune system's ability to detect and destroy cancer cells is crucial for cancer prevention and treatment. However, the role of immunosurveillance in cancer development and treatment is still debated, especially among non-immunologists and oncologists who often focus on cell-intrinsic factors. Recent studies have shown that both cell-intrinsic and cell-extrinsic mechanisms are involved in tumor suppression, and that the seventh hallmark of cancer, avoidance of immunosurveillance, is mechanistically linked to the six established cell-intrinsic characteristics of cancer cells. The immune system recognizes and destroys cancer cells through various mechanisms, including the activation of natural killer (NK) cells, T cells, and dendritic cells. However, cancer cells can evade these mechanisms by downregulating the expression of immune-related molecules, such as NKG2D ligands, or by producing immunosuppressive factors, such as IL-10 and TGF-β. The presence of tumor-infiltrating T cells (TILs) is a useful prognostic marker in several cancers, including melanoma, ovarian carcinoma, and colon carcinoma. However, the antitumor activity of these T cells can be inhibited by regulatory T cells (TReg cells) and immunosuppressive enzymes produced by tumor cells. The role of immunosurveillance in the suppression of human cancer is supported by the finding that immunodeficiencies predispose patients to the development of cancer. Patients with Chediak–Higashi syndrome, an autosomal recessive disorder that affects NK cell function, have a significantly higher risk of developing malignancy. Additionally, certain genetic polymorphisms, such as those affecting CD95L and KIRs, are associated with an increased risk of cervical cancer. The presence of certain human NKG2D alleles is also associated with a risk of developing cancer at any site. The evidence indicates that cell-intrinsic responses that participate in the suppression of tumors are linked to the expression of immunostimulatory NKG2D ligands and, perhaps, to the modulation of TRAIL-dependent apoptosis. The six cell-intrinsic hallmarks of cancer include self-sufficiency in growth signals, insensitivity to antiproliferative signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. These hallmarks are closely related to the mechanisms of immunosurveillance and immunosupversion. The seventh hallmark of cancer, avoidance of immunosurveillance, is mechanistically linked to the six established cell-intrinsic characteristics of cancer cells.Cancer immunosurveillance is the process by which the immune system recognizes and eliminates cancer cells. However, cancer cells can avoid this process through immunoselection (selection of non-immunogenic variants) and immunosupversion (suppression of immune responses). The immune system's ability to detect and destroy cancer cells is crucial for cancer prevention and treatment. However, the role of immunosurveillance in cancer development and treatment is still debated, especially among non-immunologists and oncologists who often focus on cell-intrinsic factors. Recent studies have shown that both cell-intrinsic and cell-extrinsic mechanisms are involved in tumor suppression, and that the seventh hallmark of cancer, avoidance of immunosurveillance, is mechanistically linked to the six established cell-intrinsic characteristics of cancer cells. The immune system recognizes and destroys cancer cells through various mechanisms, including the activation of natural killer (NK) cells, T cells, and dendritic cells. However, cancer cells can evade these mechanisms by downregulating the expression of immune-related molecules, such as NKG2D ligands, or by producing immunosuppressive factors, such as IL-10 and TGF-β. The presence of tumor-infiltrating T cells (TILs) is a useful prognostic marker in several cancers, including melanoma, ovarian carcinoma, and colon carcinoma. However, the antitumor activity of these T cells can be inhibited by regulatory T cells (TReg cells) and immunosuppressive enzymes produced by tumor cells. The role of immunosurveillance in the suppression of human cancer is supported by the finding that immunodeficiencies predispose patients to the development of cancer. Patients with Chediak–Higashi syndrome, an autosomal recessive disorder that affects NK cell function, have a significantly higher risk of developing malignancy. Additionally, certain genetic polymorphisms, such as those affecting CD95L and KIRs, are associated with an increased risk of cervical cancer. The presence of certain human NKG2D alleles is also associated with a risk of developing cancer at any site. The evidence indicates that cell-intrinsic responses that participate in the suppression of tumors are linked to the expression of immunostimulatory NKG2D ligands and, perhaps, to the modulation of TRAIL-dependent apoptosis. The six cell-intrinsic hallmarks of cancer include self-sufficiency in growth signals, insensitivity to antiproliferative signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. These hallmarks are closely related to the mechanisms of immunosurveillance and immunosupversion. The seventh hallmark of cancer, avoidance of immunosurveillance, is mechanistically linked to the six established cell-intrinsic characteristics of cancer cells.