Variations in the distribution of proteins that metabolize drugs can control a cancer cell's ability to respond to chemotherapeutics. The Kemp lab has used computational modeling for understanding how patient-specific variability leads to patient sensitivity to doxorubicin treatment at different doses. With this knowledge, complex behavior induced by pharmacological intervention was correctly predicted, suggesting strategies for manipulation of drug metabolism to augment cytotoxicity. The lab also investigates the role of antioxidant genes in the shift and stability of phenotypes associated with cancer cell transdifferentiation. Our most recent work has explored the dual role of antioxidant transport and drug efflux through multidrug resistance proteins in defining "cancer stem cells" known as side populations.