To establish whether regulation of autophagy in our cell models of ARSACS occurred via an mTOR dependent or independent pathway, we pre-treated cells with 3-methyladenine (3-MA), a phosphoinositide 3-kinase (PI3K) inhibitor, 3 h before treatment with carbonyl cyanide 4-trifluoromethoxyphenylhydrazone (FCCP), and analyzed expression levels of phospho-S6, an effector of the mTOR pathway, and total S6. The gene discussed is MTOR; the disease is Autosomal recessive spastic ataxia of Charlevoix-Saguenay.