For example, tumor and non‐tumor glial cells have a differential capacity to induce de novo ceramide synthesis in the ER upon cannabinoid receptor engagement and, in turn, to trigger an ER stress and pro‐autophagic response, which may determine whether the mitogenic PI3K‐Akt‐mTORC1 pathway becomes inhibited (in glioma cells) or stimulated (in non‐tumor neural cells) (Velasco et al., 2012). This evidence concerns the gene AKT1 and neoplasm.