In our model, NK cells contributed to BCG treatment success in two ways: (1) recruiting cDC1s to the tumor-bearing lung, which could be mediated by CCL5 produced by activated NK cells; (2) killing of tumor cells by BCG-activated NK cells in a perforin-dependent way, which critically generates tumor cell-derived material that is subsequently acquired by cDC1s to trigger tumor-specific T cell responses. The gene discussed is CCL5; the disease is neoplasm.