Targeted therapies offer dramatic improvements in progression free survival (PFS) for some patients. However, most patients eventually fail targeted therapy due to the emergence of drug resistance. The major genetic mechanisms of this acquired resistance are point mutations and copy number amplifications of the target gene, or amplifications of a potent, off-target oncogene that bypasses the target oncogene. Using physical parameters acquired in previous studies, our simulation shows a tradeoff between these evolutionary trajectories.