Thus, the unique property of Evobodies to activate Vγ9Vδ2 T cells by selectively triggering the BTN3A infection alarm on FOLR1 -positive tumor cells distinguishes them from pan-BTN3A activating approaches (27, 28) as well as from virtually all bispecific concepts, where the administered therapeutic antibody is – by itself – building an non-physiological, molecular bridge from the TAA/FOLR1 to an immune effector cell. Here, FOLR1 is linked to infection.