Our research is focused on the role of Ca2+ signaling in inflammation, metabolism and cancer. Activation of the Ca2+/CaM kinase cascade upon metabolic disruption is a primary driver in obesity and creates a predisposition for fatty liver disease and hepatic cancer. We are currently interrogating the role of transcriptional coregulators downstream of calcium action that drive the metabolic progression from obesity to hepatic cancer to identify potential avenues for therapeutic intervention.