Here, we selected TIM-3, LAG-3 and 2B4, three inhibitory receptors frequently expressed by T cells in several cancer types and involved in resistance to immunotherapy (32, 33), and we exploited the multiplexicity of CRISPR/Cas9 with lentiviral vectors to simultaneously redirect T cell specificity and disrupt genes encoding for TIM-3, LAG-3, or 2B4, within a protocol able to expand long-living early differentiated TSCM (34). The gene discussed is HAVCR2; the disease is cancer.