The production of αTP in vascular smooth muscle cells (VSMC) may instruct neighbouring pericytes/endothelial cells or invading monocytes/macrophages to produce VEGF leading to an increase of vascular permeability and/or adaptive formation of new vessels [62], [63], e.g. during post-infarction wound healing [64] or during development acting as tubulogenic morphogen during vasculo- and/or nephro-genesis [65]. Here, ATP8A2 is linked to infarction.