As an example, in a review article entitled “The Broad Spectrum of LMNA Cardiac Diseases: From Molecular Mechanisms to Clinical Phenotype”, Crasto and co-authors have declared that, despite the plethora of studies describing lamins’ involvement in many nuclear and cellular processes, none of these are capable, per se, in fully justifying the functional and clinical phenotypes of lamin-dependent cardiomyopathy [24], shedding light on the lack of knowledge in linking specific LMNA gene mutations to the distinct cell- or tissue-specific clinical manifestations. The gene discussed is LMNA; the disease is substance dependence.