In an in vivo Parkinson’s disease (PD) model using rotenone-mediated neurotoxicity, studies showed that sulforaphane treatment significantly modulated mTOR-mediated p70S6K and 4E-BP1-signaling pathways, inhibited neuronal apoptosis, stimulated the NRF2-dependent reduction of oxidative stress, and ultimately, was involved in the restoration of autophagy, thereby exhibiting the role of sulforaphane as a neuroprotective agent in the PD model [73]. This evidence concerns the gene NFE2L2 and Parkinson disease.