When transgenic overexpression of follistatin (F66-mice) is crossed with the dysferlinopathy LGMD2B model Dysf−/−, the positive effect on muscle weight in F66;Dysf−/−-mice declines with age and the specific force of EDL is reduced, compared to F66-mice, exacerbating the dystrophic phenotype [104]. Here, FST is linked to neuromuscular disease caused by qualitative or quantitative defects of dysferlin.