Despite pemigatinib’s failure to reduce ABCB1 expression in cancer cells and its lack of effect on ABCB1 subcellular localization, the molecular docking data demonstrated pemigatinib’s capacity to bind to the substrate-binding site of ABCB1, thereby illustrating the potential molecular mechanism by which anti-cancer drugs are retained in cancer cells [169]. The gene discussed is ABCB1; the disease is cancer.