TIMP3 clusters in the main network for extracellular matrix organization that includes ADAMTSL4, LRP1 and COL4A1, with connections with subnetworks of F3. This clustering is consistent with the biological function of TIMP3 as an inhibitor of matrix metalloproteinases with domains interacting with ADAMTS proteins and LRP1, involving proteins encoded by genes prioritized in SCAD loci40. Here, COL4A1 is linked to spontaneous coronary artery dissection.