These may present as early heart rhythm disorders without overt structural disease, isolated LV dilation, isolated scar, or hypokinetic non-dilated cardiomyopathy.7 Despite well-established genotype–phenotype correlations for specific gene variants [e.g. desmoplakin (DSP), filamin-C (FLNC), and laminin], myocardial resilience to disease progression in gene-related, familial gene elusive, acquired, and idiopathic forms remains largely unknown. This evidence concerns the gene FLNC and Arrhythmia.