Epstein-Barr Virus (EBV) is latent in 90% of the adult human population but can be deadly to those who are immunocompromised, such as in post-transplant proliferative disorder (PTLD), a potentially fatal complication to organ transplants. A complete understanding of the viral mechanisms of EBV and how it can lead to B cell lymphomas is necessary for the development of therapies. Here, we study how variation in the primary oncogene of EBV, latent membrane protein (LMP)1, can affect the expression of cellular proteins. LMP1 is a mimic of the B cell co-stimulatory membrane protein CD40 required for B cell differentiation and activation. Different genetic variants of LMP1 differentially regulate microRNA-193b (miR-193b), a post-transcriptional regulator known to target three target genes implicated in tumorigenesis: MCL1 (MCL1), TSC1 (TSC1), and CCND1 (Cyclin D1). Here we study whether LMP1 regulates the expression of miR-193b targets MCL1, TSC1, and Cyclin D1 in B cells. To answer this question, we used a chimerically inducible model of LMP1 signaling using two LMP1 variants: B95.8 lab variant and a variant isolated from a patient with EBV+ PTLD (tumor variant). Previously, we showed that the B95.8 LMP1 but not tumor variant LMP1 regulates the expression of microRNA-193b (miR-193b). We hypothesized that after B95.8 LMP1 activation, expression of miR-193b target proteins would be decreased, but after activation of tumor variant LMP1, miR-193b target protein expression would not change. First, we used flow cytometry to analyze whether a NGFR.LMP1 model of LMP1 signaling was expressed and functional in EBV- BL41 B cells. Additionally, we determined the optimal conditions to detect MCL1, TSC1, and Cyclin D1 by Western blot. We were unable to detect Cyclin D1 by Western blot and were thus unable to include it in further analysis. After activation of LMP1 by crosslinking of NGRF.LMP1, we analyzed the expression of MCL1 and TSC1 with Western blots and quantified expressing using densitometry analysis. We found that after LMP1 activation, B cells transfected with B95.8 LMP1 decreased expression of TSC1 and significantly decreased expression of MCL1, but B cells transfected tumor variant LMP1 did not have altered expression of MCL1 or TSC1. These results indicate that genetic variation in EBV LMP1 leads to differential regulation of miR-193b target proteins MCL1 and TSC1.