Given the limited brain exposure of repotrectinib found in wild-type mice because of Abcb1a/1b and Abcg2 functions, and their potential clinical relevance for limiting therapeutic efficacy against brain malignancies as well as tumor cells that themselves express ABC transporters, we could consider to use this insight to enhance the CNS (and tumor) exposure of repotrectinib by the application of potent pharmacological ABCB1 and ABCG2 inhibitors such as elacridar. The gene discussed is ABCB1; the disease is neoplasm.