The proposed model of GS-mediated apoptosis in HNSCC cells. Our results demonstrated GS targets 14-3-3 zeta to initiate apoptosis through the intrinsic mitochondrial pathway by releasing Bad from its inhibitory action. Activation of PP2A inhibited association of Bad with 14-3-3 zeta resulting in its accumulation on outer mitochondrial membrane, altering its membrane potential. This releases cytochrome c, activating the downstream caspases - caspase 9 and caspase 3. In addition, treatment with GS induces expression of CD95/Fas receptors leading to caspase 8 activation in head and neck cancer cells.