Thus, we evaluated whether LHON mutations alter the mTOR/AMPK pathway by assessing AMPK phosphorylation levels and the regulation of mTOR-downstream targets, including the phosphorylation/inactivation of the mRNA translation repressor 4E-binding protein (4EBP1) and the autophagy regulator Unc-51 like autophagy activating kinase (ULK1), a serine/threonine (Ser/Thr) kinase that plays a specific role in clearing mitochondria (Egan et al., 2011). The gene discussed is MTOR; the disease is Leber hereditary optic neuropathy.