In models of DCM and left ventricular non-compaction (LVNC) caused by gene mutations, mutations in Pleckstrin homology domain containing M2 (PLEKHM2) lead to abnormal accumulation of Rab5, Rab7, and Rab9-positive endosomes, affecting lysosomal positioning and ultimately disrupting autophagic flux (64). The gene discussed is RAB7A; the disease is familial dilated cardiomyopathy.