The implementation of the studies concerning the role of thymus in mediating dystrophic pathogenesis could lead to an understanding of whether DMD patients’ T cell development is impaired by specific dystrophin-mutations and whether defective T-cell proliferation could be rescued by specific genetic manipulation or the in vitro modulation of patient source cells that partly counteract thymic abnormalities. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.