Familial Hemophagocytic Lymphohistiocytosis (HLH) is a biallelic genetic disorder that may cause disruptions in the assembly and transport of perforin-containing granules in CD8 T-Cells and NK Cells, and this lack of perforin-containing granules may result in reduced cytotoxicity and hyperinflammation. Current methods for detecting HLH in patients are poor due to the prolonged length of genetic testing and the high rate of false positives for NK Cell chromium-51 assays. Measuring cytotoxicity from CD8 T-Cells is ideal due to their prominent role in fighting infections as they occur, but the antigenic specificity of T-Cell receptors has made developing an assay difficult. Blinatumomab, a bispecific monoclonal antibody developed to combat B-Cell acute lymphoblastic leukemia (ALL), may offer a potential solution. Through its anti-CD3 and anti-CD19 portions, it can join any CD8 T-Cell with a B Cell. This triggers the CD8 T-Cell to release its granules and induce cell apoptosis while ignoring the T-Cell receptor’s antigenic specificity. Thus, we aimed to develop an assay for detecting HLH by co-culturing CD8-T-Cells obtained from their blood with B-Cells in the presence of Blinatumomab. We hypothesized that the memory T-cells from HLH patients with granule-mediated cytotoxicity mutations will have a prolonged immune synapse duration and increased production of cytokines when compared to functional memory T cells.    To develop this assay, CD8 T-cells were isolated from a blood sample and were transfected with siRNA. One portion of the cells was transfected with siRNA that silenced the expression of perforin to simulate the phenotype of an HLH patient and the other with siRNA, which did not silence the expression of any protein, to simulate the phenotype of a non-HLH patient. Through RNA extraction, cDNA amplification, and qPCR, the expression of perforin was measured for both groups. Then, these CD8 T-Cells were co-cultured with Nalm6 cells (a B Cell precursor to ALL) and Blinatumomab in a killing assay. From the results of the killing assay, we found a substantial difference in the cytotoxicity between the T-Cells with functional perforin and the T-cells that lacked perforin, which indicates promise in using Blina to detect HLH from a killing assay performed on CD8 T-Cells. For future research, the cytotoxicity of CD8 T-Cells obtained directly from the blood samples of HLH patients should also be measured in a killing assay with Nalm6 and Blinatumomab to determine if this potential assay can detect a difference in cytotoxicity for non-simulated HLH.