Inhibition of DGAT1 was shown to significantly upregulate the carnitine palmitoyltransferase 1A (CPT1A) protein, which facilitates the entry of excessive fatty acids (FAs) into the mitochondria for oxidation, resulting in mitochondrial damage, remarkable increase in GBM cell apoptosis, and ROS production (Cheng et al., 2020). The gene discussed is CPT1A; the disease is glioblastoma.