“…Indeed, CMA is essential in Parkinson’s disease where its dysregulation modifies the onset or progression of the disease (Arias and Cuervo, 2011 ; Cuervo, 2011 ; Alfaro et al, 2018 ; Kaushik and Cuervo, 2018 ). Alpha-synuclein protein, leucine-rich repeat kinase 2 (LRRK2), Parkinson disease protein 7 (PARK7), and DJ-1, as well as myocyte-specific enhancer factor 2D protein (MEF2D), which are dysregulated or mutated in Parkinson’s disease, are CMA substrates (Vogiatzi et al, 2008 ; Yang et al, 2009 ; Arias and Cuervo, 2011 ; Cuervo, 2011 ; Orenstein et al, 2013 ; Murphy et al, 2015 ; Alfaro et al, 2018 ; Kaushik and Cuervo, 2018 ). Alzheimer’s disease is also associated with CMA since the beta-amyloid peptide (Aβ), the microtubule-associated protein Tau or the Regulator of calcineurin 1 (RCAN1) are involved in Alzheimer’s disease and are dysregulated when CMA is altered (Liu et al, 2009 ; Wang et al, 2009 , 2010 ; Park et al, 2016 ).…”