Selective cytotoxicity against OSCC cells; showed cell-cycle arrest, by increasing the expression of cyclin-dependent kinase inhibitors (CDKIs) such as p21, p27, p16 or p53 and Rb (retinoblastoma protein); reduce DNA damage on oral cancer cells by inhibition of H2A.X protein expression; induces autophagy, reduces reactive oxygen species, increases intracellular glutathione activity and decreases mitochondrial membrane potential in cancer cells; potential as a therapeutic agent for oral cancer [241]. This evidence concerns the gene CDKN2A and lip and oral cavity carcinoma.