The overarching goal of our research program is to understand the role of mitochondrial calcium signaling in physiology and pathology. We recently showed that a mitochondrial calcium signaling is activated in the rare pediatric liver cancer fibrolamellar carcinoma (FLC). This activation leads to metabolic changes in FLC that we hypothesize to promote cancer growth. One major limitation we face in our FLC work is lack of disease models. Mouse models failed to recapitulate many aspects of the disease, likely due to metabolic differences between mouse and human liver metabolism. Similarly, patient derived cells are not adequate disease models. We are interested in overcoming this limitation by using patient-derived induced pluripotent stem cells (iPSCs). In the long term, we are interested in differentiating iPSCs that we will generate into hepatocytes or cholangiocytes as FLC models. Such models will enable us to better understand disease mechanisms, and search for therapeutic avenues for this debilitating cancer.