Thus, we could consider that in MJD patients sequestration of normal ATX3 into the aggregates might lead to decreased levels of α5β1 and α7β1 integrin levels and, thereby, to an impairment of myogenesis either during development or in adult MSCs, that differentiate and give rise to new muscle fibers upon muscle injury, possibly leading to the muscle atrophy seen in some type III MJD patients [31], [32]. This evidence concerns the gene ATXN3 and Machado-Joseph disease.