AXL and atherosclerosis: Accordingly, during aging or in pathological conditions including chronic kidney disease (CKD), atherosclerosis or type 2 diabetes (T2D), the molecular mechanisms that promote VSMCs senescence, like prelamin A accumulation [16] or cartilage oligomeric matrix protein (COMP) [17], sirtuin 1 (SIRT1) [18] and AXL receptor tyrosine kinase (Axl) [19] downregulation, support their osteogenic transdifferentiation and VC.