One such study discovered the dependency of highly aggressive human lung adenocarcinomas, harboring KEAP1 mutations that overactivate NRF2, on solute carrier family 33 member 1 (SLC33A1), an endomembrane-associated protein involved in autophagy regulation, which can be used to develop targeted therapies for this type of cancer [24]. This evidence concerns the gene KEAP1 and lung adenocarcinoma.