Commonly, the mutation that causes FPLD2 affects exon 8 (replacement of arginine by a neutral amino acid at position 482 - R482W), but other mutations in exon 8 and 11 (codon 644 - R644C) have already been described.6,7 It has been shown that the LMNA R482W mutation is more associated with muscle and cardiac abnormalities, such as muscular atrophy and dystrophy, cardiac hypertrophy and advanced atherosclerosis.8 But the phenotypic differences associated with each specific mutation determinant of FPLD are yet to be elucidated. Here, LMNA is linked to muscular atrophy.