Our data show that a bivalent VHH that links a high and low affinity Vδ2-TCR specific VHH can support Vγ9Vδ2 T-cell expansion in vitro, ex vivo and in vivo and that this ability is maintained when incorporated in bispecific formats, allowing lysis of TAA expressing tumor cells, also in combination with an Fc domain or anti-albumin binding unit for plasma half-life extension. The gene discussed is ALB; the disease is neoplasm.