Our findings show that loss of genes in the von Hippel–Lindau (VHL) tumor suppressor and the mammalian target of rapamycin complex 1 (mTORC1) pathways confers resistance to acute IMT1 treatment, whereas further impairment of mitochondrial function, such as inhibition of mitochondrial translation and reduction of mtDNA copy number, increases sensitivity to IMT1 treatment. This evidence concerns the gene VHL and neoplasm.