In GBM, the antioncogenic perspective of luteolin has been correlated with its capacity to inhibit cell growth, to induce apoptosis, to slow down and reduce invasion and migration, and to downregulate iNOS expression, proved on human glioblastoma T98G (mutant p53) and U87MG (wild-type p53) cancer cell lines [12]. The gene discussed is TP53; the disease is glioblastoma.