University of California, San Francisco researchers discovered that tumor cells carrying KRAS gene mutations accumulate large amounts of a reactive form of iron, and that this “ferroaddiction” can be exploited to specifically deliver anticancer drugs to the ferroaddicted tumors without harming normal, healthy cells. For their reported study the team tweaked an anticancer drug, cobimetinib, to generate a ferrous iron-activatable drug conjugate (FeADC), which effectively inhibited tumor growth in animal models.