Arriga R, Caratelli S, Lanzilli G, et al. - Since KRAS-mutated cancer cell growth in vitro is inhibited by cetuximab, via NK cell-mediated antibody-dependent-cellular-cytotoxicity but KRAS-mutated colorectal carcinoma (CRC) cells escape NK cell immunosurveillance in vivo, researchers wanted to overcome this limitation. In this study, cetuximab and panitumumab were used to redirect Fcγ chimeric receptor (CR) T cells against KRAS-mutated HCT116 CRC cells. Comparisons were performed between four polymorphic Fcγ-CR constructs (CD16^158F-CR, CD16^158V-CR, CD32^131H-CR, and CD32^131R-CR) transduced into T cells by retroviral vectors. The killing of HCT116 cells and A549 KRAS-mutated cells in vitro was induced by only CD16^158V-CR T cells combined with cetuximab. In CB17-SCID mice in vivo, subcutaneous growth of HCT116 cells was successfully controlled by CD16158V-CR T cells. Overall, the utility of CD16^158V-CR T cells combined with cetuximab was suggested as reagents for the development of innovative epidermal-growth-factor-receptor+KRAS-mutated CRC immunotherapies.