Natural Killer (NK) cells are innate immune cells that play a crucial role in the first line of defense against cancer. They recognize and destroy abnormal cells, contributing to immunosurveillance. NK cells utilize cytotoxic granules, death receptors, and cytokines to eliminate cancer cells. They also interact with other immune cells in the tumor microenvironment, influencing the anti-tumor response. NK cells are classified into two subsets: CD56bright (CD16-) and CD56dim (CD16+), with distinct functions. CD56bright NK cells are more cytokine-producing, while CD56dim NK cells exhibit stronger cytotoxicity. NK cells can be activated through various receptors, including NCR, NKG2C, DNAM1, and CD16a, which mediate cytotoxicity and ADCC. NK cells also release lytic granules containing perforin, granzyme B, and granulysin, which induce apoptosis in target cells. Additionally, NK cells can trigger apoptosis through death receptors like FasL and TRAIL. Cytokines such as IFNγ and TNF-α produced by NK cells enhance immune responses and tumor cell death. NK cells interact with other immune cells, including macrophages, dendritic cells, and T cells, modulating their functions and contributing to anti-tumor immunity. However, the tumor microenvironment can impair NK cell activity through immunosuppressive factors and cells. Understanding NK cell mechanisms and interactions is essential for improving NK-based therapies in cancer treatment.Natural Killer (NK) cells are innate immune cells that play a crucial role in the first line of defense against cancer. They recognize and destroy abnormal cells, contributing to immunosurveillance. NK cells utilize cytotoxic granules, death receptors, and cytokines to eliminate cancer cells. They also interact with other immune cells in the tumor microenvironment, influencing the anti-tumor response. NK cells are classified into two subsets: CD56bright (CD16-) and CD56dim (CD16+), with distinct functions. CD56bright NK cells are more cytokine-producing, while CD56dim NK cells exhibit stronger cytotoxicity. NK cells can be activated through various receptors, including NCR, NKG2C, DNAM1, and CD16a, which mediate cytotoxicity and ADCC. NK cells also release lytic granules containing perforin, granzyme B, and granulysin, which induce apoptosis in target cells. Additionally, NK cells can trigger apoptosis through death receptors like FasL and TRAIL. Cytokines such as IFNγ and TNF-α produced by NK cells enhance immune responses and tumor cell death. NK cells interact with other immune cells, including macrophages, dendritic cells, and T cells, modulating their functions and contributing to anti-tumor immunity. However, the tumor microenvironment can impair NK cell activity through immunosuppressive factors and cells. Understanding NK cell mechanisms and interactions is essential for improving NK-based therapies in cancer treatment.