These gene mutations, considered independent pathogenic agents for muscle diseases, include SUN1/2, which are viewed as disease-modifying genes for other causative genes of EDMD, such as LMNA, EMD, and LAP2α [16, 27].Nesprin mutations variably impact LINC complex functions, particularly in the C-terminal SR region, inducing nuclear morphology defects and disrupting binding with nuclear membrane-associated proteins. The gene discussed is EMD; the disease is Emery-Dreifuss muscular dystrophy.