Multiple sclerosis (MS) is a chronic multi- faceted demyelinating and neurodegener- ative disease of the central nervous system (CNS) of presumed autoimmune origin.1 Patients with MS are characterised by a spatial and temporal dissemina- tion of neurological sign and symptoms, by the presence of multifocal lesions in the periventricular white matter on MRI scans and by an immunoglob- ulin synthesis within the CNS.1 Further diagnostic tools are desirable, and the use of blood and cerebrospinal fluid (CSF) biomarkers may contribute to the comprehension of the disease’s patho- genesis and progression. Autophagy is an evolutionarily conserved and genetically controlled cellular process where intracellular compo- nents are sequestered within double-mem- brane vesicles (autophagosomes), which then fuse with lysosomes where the mate- rial is degraded.2 Autophagy also occurs as mitophagy, which is responsible for the removal of aberrant, aged and wasted mitochondria. Interestingly, autophagic/ mitophagic pathways have been found deregulated in various human diseases. In particular, it has been demonstrated how these catabolic pathways are implicated in several neurodegenerative diseases such Alzheimer’s and Parkinson’s diseases and amyotrophic lateral sclerosis.2 Moreover, recent studies suggest a role of mitochon- drial dysfunction in the neurodegenerative aspects of MS.3 Despite these observa- tions, the role of autophagy and mito- phagy in MS is still elusive. To tackle the question, we tried to verify the frequency of specific autophagic markers (ATG5 protein) and mitophagic markers (Parkin protein) in patients with MS and in neurological controls.