Interestingly, most mutations in patients with FPLD occur in the carboxy terminal domain of lamin A/C, while cardiomyopathy has been associated with mutations in amino terminal domain of the lamin A/C in FPLD patients.2 Several heterozygous mutations in LMNA like the R28W, R60G, R62G, and D192V have been reported to be associated with lipodystrophy and cardiomyopathy. This evidence concerns the gene LMNA and familial partial lipodystrophy.