To explore the generalizability of this IFITM-promoted cellular uptakemechanism, we designed, synthesized, and characterized a bitopic inhibitor thatis, aside from being a linked molecule, compositionally unrelated to RapaLink-1.This inhibitor targets a different intracellular protein, BCR-ABL1, a fusiononcoprotein associated with CML and other leukemias (52). Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.