In mouse models, SLC7A5 was upregulated in oncogenic KRAS-mutant colorectal cancer cells [14]; SLC7A5 helped maintain intracellular amino acid levels and supported the increased protein synthesis that underpins the enhanced KRAS-mutant cell proliferation, whereas targeting protein synthesis via mTOR regulator and SLC7A5 abrogated the growth of established KRAS-mutant tumors [15]. This evidence concerns the gene KRAS and colorectal cancer.