**7.1. Chemicals that will initiate the recovery of mitochondria**

Our previous *in vitro* studies showed that Rsv moderately upregulates the expression of various duplicated GGAA-motif-driven genes, including *TP53* and *HELB* [46, 48, 78]. Given that the increase in the NAD+ /NADH ratio can improve the mitochondrial functions, the introduction of the redox reaction-associated genes may be applied in cancer treatment. PARP inhibitors, which are especially effective for treating cancer with BRCA1 and BRCA2 mutations by disrupting specific types of DNA repair systems, are clinically approved drugs [89]. Another compound is TEMPOL, an antioxidant that has a suppressive effect on tumor cell proliferation [178], which increases the cellular NAD+ level, supporting the DNA repair system [179, 180]. A number of compounds that target mitochondria have been tested in clinical trials [181]. Tocotrienols and their analogues target mitochondria and the immune system, causing the death of cancer cells [182]. Metformin and rapamycin are also expected to be novel anti-cancer/aging drugs that effectively suppress mTOR signaling [183]. Activators of mTOR, AMPK, and PGC-1α have been shown to have a synergistic effect with PD-1 blockade therapy [184], suggesting that mitochondrial activation can augment the immune response.
