Hispidulin has been indicated with diverse mechanistic insights in cell cycle arrest: in gastric cancer AGS cells, it sustains NAG-1 (NSAID-activated gene-1) expression through ERK activation, followed by the downregulation of cyclin D1/E, and eventually induces G1/S arrest with apoptosis (Yu et al., 2013; Lin et al., 2010); in glioblastoma multiforme (GBM) cells, it activates AMPK, thereby inhibiting the downstream mTOR expression, and thus upregulating p53/p21 to block G1 progression (Ishikawa et al., 2008). The gene discussed is TP53; the disease is glioblastoma.