So, there are two different approaches: on the one hand, RAF inhibitors such as sorafenib seem to be potent induction for the pre-activation of NK cells, on the other hand, in vitro pre-treatment with clinically relevant concentrations of sorafenib leads to impaired NK-cell effector functions [106] and higher doses of sorafenib might lead to immunosuppression and reduced anti-tumor response by NK cells in vivo [101, 107, 108]. The gene discussed is RAF1; the disease is neoplasm.