Upon treatment of ibrutinib plus etomoxir, the carnitine palmitoyltransferase I (CPT-1) inhibitor suppressing β-oxidation of fatty acids in mitochondria, GLUT1 expression and glucose uptake in resistant chronic lymphocytic leukemia (CLL) cells were decreased compared to sensitive cells, suggesting the activation of fatty acid oxidation might be important for the sustenance of ibrutinib resistance in CLL cells [24]. The gene discussed is CPT1C; the disease is B-cell chronic lymphocytic leukemia.