We recently showed that excessive and sustained activation of the DNA damage response (DDR) and poly-ADP ribose polymerase 1 (PARP1) signaling is a major characteristic of the ‘local’ component of PXE pathophysiology, and that targeted inhibition of PARP1 by minocycline significantly attenuates ectopic calcification in PXE cells and tissues [12]. The gene discussed is PARP1; the disease is Pseudoxanthoma elasticum.