While it is well appreciated that endothelial dysfunction leads to cardiovascular remodeling and deregulated angiogenesis, very little is known about the mechanisms of progerin‐induced angiogenic incompetence in HGPS. Since HGPS is a very rare disease, and because the patients are very frail, it is challenging to obtain patient‐derived tissue‐specific cell lines to study HGPS disease mechanisms (Gordon et al., 2014). This evidence concerns the gene LMNA and endothelial dysfunction.