Activating KRAS mutations deregulate mitosis, nuclear export, redox, and mitochondrial activity, and KRAS-mutant cancer cells have consequently been shown to have a greater dependency on the functions of non-oncogenes [e.g., PLK1, XPO1, and MRPL52 (a component of the mitochondrial large ribosomal subunit)] that play critical roles in their respective processes [12–16], suggesting that targeting non-oncogene addiction is an attractive approach for the treatment of KRAS-mutant cancer [17, 18]. Here, XPO1 is linked to cancer.