In support of this observation, we further demonstrated that TGFBR2 knock-out NK cells experience lower levels of SMAD2/3 phosphorylation than control unedited NK cells after stimulation with 10 ng/mL TGF-β (Supplementary Fig. 13a), providing a biochemical mechanism to support the functional improvement observed in tumor killing assay (Fig. 6C). The gene discussed is TGFB1; the disease is neoplasm.