For example, Spectrin binds α-Synuclein leading to Actin dynamic impairments and mitochondria loss of function through delocalization of Drp1; in mice and post-mortem human brains with α-Synucleinopathy, it was shown that Spectrin overexpression rescues α-Synuclein toxicity and restores cytoskeletal architecture homeostasis, demonstrating that α-Synuclein/Spectrin association causes Actin filaments’ pathogenic changes and leads to consequent neurotoxicity, and offering a new potential therapeutic target (Figure 6b) [201]. The gene discussed is DNM1L; the disease is synucleinopathy.