For the treatment of cisplatin-induced AKI [33], regulation on cisplatin-induced cell death by targeting Bax [34] and p53 activation [35], cell senescence and growth arrest by targeting JNK [36] and p38 MAPK [37], endoplasmic reticulum stress by targeting PERK and CHOP [38], autophagy by targeting mTOR [39], and immune cell activation by targeting CD4 positive T cells [40] and TNF-α [41] are proposed. Here, BAX is linked to acute kidney injury.