Alterations to the interactions between LTBP4 and tropoelastin and fibulin-4 would likely perturb normal elastogenesis contributing to ARCL1C pathogenesis where abnormal elastin aggregates are incorrectly incorporated into fibrillin microfibril scaffolds. The gene discussed is ELN; the disease is cutis laxa with severe pulmonary, gastrointestinal and urinary anomalies.