The number of deaths from cancers attributable to the Epstein-Barr Virus (EBV), such as EBV+ B cell lymphomas, is steadily increasing. Elucidation of the viral mechanisms that underlie the development of EBV+ B cell lymphomas could help to identify potential therapies. EBV is a ubiquitous herpesvirus that can alter the expression of host B cell genes, including microRNAs (miRs). miRs are post-transcription regulators that degrade mRNA or inhibit translation of target mRNA. The broad aim of this study was to elucidate how the primary oncogene of EBV – LMP1 – regulates host B cell miRs. Our preliminary data indicate that LMP1 upregulates miR-155 via PI3K p110α. Moreover, the miR-155 target and tumor suppressor – SHIP1 – was not downregulated in EBV+ B cell lymphomas. To determine if LMP1 regulates expression of miR-155 target SHIP1 via PI3K p110α, we utilized EBV- B cell lymphoma lines that stably expressed chimeric NGFR.LMP1 molecules. NGFR.LMP1 has the extracellular transmembrane domains of nerve growth factor receptor (NGFR) and the C-terminus tail of LMP1 that contains its signaling domains. To ensure that the NGFR.LMP1 molecules were functional, we measured intracellular adhesion molecule (ICAM) and miR-155 levels after inducing LMP1 signaling by crosslinking NGFR.LMP1 molecules using mouse anti-NGFR and then goat anti-mouse antibodies. We observed a significant increase in both ICAM and miR-155, which supports that we have a functional model. We then activated LMP1 in the presence of a PI3K p110α inhibitor, BYL719, and measured expression of SHIP1 by Western blot. When LMP1 signaling is activated, SHIP1 expression significantly decreased, suggesting that LMP1 regulates SHIP1. Additionally, BYL719 treatment did not significantly rescue SHIP1 levels, which indicates that although LMP1 regulates SHIP1, LMP1 does not do so via activation of PI3K p110α. A future direction is to confirm these findings by knocking down PI3K p110α. Altogether, our data suggest LMP1 regulates expression of the miR-155 target SHIP1, but not via activation of PI3K p110α. Further study is needed to understand how SHIP1 is regulated. In sum, this mechanism suggests that miR-155 and SHIP1 may be potential therapeutic targets for EBV+ B cell lymphomas.