The transcriptional and the metabolic programs of a cell are two fundamental sets of instructions that dictate the behavior of the cell, the functions performed by the cell, and how the cell responds to various stimuli. These two programs interact with one another and change in response to physiochemical stimuli, enabling the cell to restore cellular homeostasis. Permanent alteration to these cellular programs contributes to the development of various pathologic conditions. Our research focuses on characterizing the mechanisms by which these pathologic alterations arise. Computational analyses of omics data and computational modeling allow us to quantify changes (both pathologic and non-pathologic) to these cellular programs and to predict the mechanisms by which those changes occur. The predictions made through the computational methods can then be tested using the tools of biochemistry and of molecular genetics. A mechanistic understanding of how pathologic alterations to the cellular transcriptional and the cellular metabolic programs occur is the key to disease management and therapeutic development.