Elimination of myostatin in the dy(W) laminin alpha2-deficient murine model of congenital muscular dystrophy was associated with increased pre-weaning mortality, potentially due to reduced fat formation [22], while blockade of myostatin with transgenic expression of follistatin in the Dyf−/− model of LGMD2B and Myoshi myopathy exacerbated muscle degeneration with aging [23]. The gene discussed is MSTN; the disease is congenital muscular dystrophy due to LMNA mutation.