Furthermore, reduced levels of BST-2upon lysosomal degradation prevent the release of EGFR from lipidrafts, which immediately affects downstream signaling and proliferation.Overall, BST-2 represents a promising hot spot for therapeutic approaches,as it drives the activity of the crucial downstream EGFR pathway.Pharmacologically fine-tuned NCA derivatives switching on the degradationof aberrantly expressed BST-2 in cancer cells represent a novel andeffective treatment option. This evidence concerns the gene BST2 and cancer.