Fernández et al. (2016) show that increasing intracellular iron causes EL alterations associated with impaired autophagic clearance, increased cytosolic oxidative stress, and increased cell death and these effects are subject to NAADP. Cell death triggered by altered intralysosomal iron handling is abrogated by inhibiting RAB7A activity. Alterations in the activity of Rab7 may be associated with cardiovascular diseases, lipid storage disorders, and neurodegenerative diseases (Cataldo et al., 2008; Zhang et al., 2009; He et al., 2019). This evidence concerns the gene RAB7A and cardiovascular disorder.