B cell lymphocytes are an immune cell able to generate antigen specific responses. B cell activation occurs through two different receptors, the B cell receptor and CD40, by interaction of antigen and CD40 Ligand, respectively. Following activation through the BCR and CD40, B cells undergo the energetically demanding processes of proliferation and differentiation into either memory cells, which provide a rapid and strong response to a secondary infection, or plasma cells, that produce large amounts of antigen specific antibodies. The immune cell most similar to B cells – T lymphocytes – require a metabolic change to aerobic glycolysis following activation to support effector function and memory differentiation. Due to the similarities in effector and memory classes of the two cell types, we hypothesized that a metabolic change must also occur in B cells to allow for their proliferation and differentiation to memory cells. Specifically, we examined alterations in mitochondrial mass to indicate a metabolic transition after activation. To do this, we stained cells with MitoTracker Green stain and quantified mitochondrial content by flow cytometry. We previously demonstrated that mitochondrial mass increased following stimulation through the BCR and CD40 in the Ramos cells – a germinal center-like Burkitt’s Lymphoma B cell. To generalize these results, we repeated these experiments in BL41, another Burkitt’s lymphoma B cell line. However, we found no increase in mitochondrial mass in BL41 following stimulation through BCR and CD40. We therefore investigated if strength of signaling could effect the cell types differently, and preliminary data suggests that increased BCR stimulation in BL41 may increase mitochondrial mass. We also asked whether a viral CD40 mimic – the Epstein-Barr Virus (EBV) protein LMP1 – can regulate mitochondrial mass in BL41 cells. LMP1 signaling did not increase mitochondrial mass. These results could motivate future studies investigating the mechanism through which mitochondrial mass increases in Ramos cells in response to BCR and CD40 activation, using BL41 as a negative control.