TCR-engineered cells can be powerful tools in the treatment of malignancies. In contrast to CAR-engineered cells, TCR-engineered cells can recognize intracellular peptides presented in HLA-class I molecules, thereby broadening the potential tumor specific targets. One potential target candidate for TCR therapy in Multiple Myeloma is BOB1, a transcription factor highly expressed in all healthy and malignant B-cell lineages. Previous research showed that Multiple Myeloma cells cannot survive when BOB1 is not expressed, which prevents immune escape of the tumor cells by downregulating this target. However, tumor-resistance by HLA-class I downregulation can still negatively-impact the success of any TCR-mediated cell therapy. To overcome this, TCR therapy can be combined with NK therapy. Allogeneic NK-cells have demonstrated efficacy and safety against malignancies without inducing GvHD highlighting the feasibility for an “off the shelf” cellular therapeutic. They are capable of recognizing HLA-negative tumors, using a broad array of intrinsic activation mechanisms. However, expansion and survival of NK cells relies on the presence of cytokines, especially interleukin-15. This dependence on interleukin-15 may hamper NK cell persistence in vivo and consequently, the success of NK cell therapies. In here, we combined the anti-tumor effector functions of NK cells with TCR-engineering (NK:TCR), producing endogenous soluble interleukin-15, creating a novel therapeutic strategy to avoid TCR-associated immune resistance.