It has been widely proposed that LMNA deletion or mutation can cause weakness of the nuclear lamina skeleton protein and structure, damage to the cardiomyocyte coding sarcomere or Ca2+ processing protein, and lead to cardiomyocyte apoptosis and abnormal contractile function, which has been implicated in disease progression in DCM and arrhythmias (Nikolova et al., 2004; Su et al., 2022; Chatzifrangkeskou et al., 2023). This evidence concerns the gene LMNA and familial dilated cardiomyopathy.