Indeed, pharmacological activation of AMP-activated protein kinase (AMPK), a known activator of autophagy, and stimulation of transcription factor EB (TFEB), a transcription factor that drives transcription of autophagic machinery, implicates dysfunctional autophagy as part of the dystrophic disease process, but also demonstrates the potential therapeutic value of increased autophagy for dystrophin deficiency (Ljubicic et al., 2012; Pauly et al., 2012; Spaulding et al., 2020a). Here, TFEB is linked to neuromuscular disease caused by qualitative or quantitative defects of dystrophin.