The regulation of ECM deposition was the main impaired pathway in our LRP1 knockout iPSC-SMCs, a key pathway in several arterial diseases that are specifically suspected in the case of FMD and SCAD.55,56 To investigate further this mechanism, we assayed changes using label-free quantification with MaxQuant software40 of ECM composition by mass spectrometry of decellularized extracts of LRP1 knockout and WT iPSC-SMCs. The gene discussed is LRP1; the disease is spontaneous coronary artery dissection.