For the first time, this study demonstrated that the neuroprotective action of 3,3′-diindolylmethane against ischemia involves an inhibition of apoptosis and autophagy and depends on AhR/CYP1A1 signaling and HDAC activity, thus providing prospects for the development of new therapeutic strategies that target neuronal degeneration at specific molecular levels. The gene discussed is AHR; the disease is ischemia.