In addition to the action of 4-dmH on SIRT1, its preferential targeting of tNOX resulted in greater therapeutic efficacy in diminishing oral cancer cell proliferation and inhibiting tumor growth by inhibiting tNOX activity, increasing its protein degradation, and ultimately provoking apoptosis in p53-functional and p53-mutated oral cancer systems (Figure 10f). Here, ENOX2 is linked to neoplasm.