We previously showed that (i) mortalin is mainly localized in mitochondria in MTC cells [13]; (ii) that mitochondrial damage was a key mechanism by which mortalin depletion suppressed MTC cells [13]; and (iii) that interfering with mitochondrial redox and bioenergetics using the mitochondria-targeted agent, Mito-CP, was as effective as mortalin depletion in suppressing MTC cells [14,15,16]. The gene discussed is HSPA9; the disease is medullary thyroid gland carcinoma.