Furthermore, SOD2 appears to be down-stream of PKCe signaling in non-muscle cells: (i) in a lung adenocarcinoma cell line, TPA (12-O-tetradecanoylphorbol-13-acetate) up-regulated PKCe- and PKCalpha-dependent transcriptional pathways to induce SOD2 expression [60] and (ii) in primary human hippocampal neuron cultures, the loss of PKCe reduced SOD2, resulting in oxidative stress, and these effects were reverted by the PKCe activator bryostatin in a murine model of Alzheimer’s disease [61]. The gene discussed is PRKCE; the disease is lung adenocarcinoma.