Since Bi-7D6-Fab surpassed 7D6 F(ab’)2 and mAb capacity to drive T cells into fratricide while overriding cell proliferation in vitro (Figures 2, 3, 4), as well as in vivo in the absence of cytokine release syndrome (Supplementary Table S2), developing recombinant anti-TCR and/or anti-CD3 Bi-Fabs functionally bivalent might deliver a more efficient and safer strategy to remove pathogenic T cells when aiming to prevent progression of autoimmune diseases such as T1D, or graft rejection upon organ transplantation, than current anti-CD3 Fc-containing Igs. The gene discussed is CUBN; the disease is type 1 diabetes mellitus.