We hypothesize that the reported differences are explained by the cellular source and time point of Cxcl4 expression: In systemic sclerosis, continuous production of CXCL4 by pDC may drive capillary rarefaction, while in ischemic organ injury short-term local exposure to platelet- or monocyte-derived CXCL4 drives fibrosis via profibrotic macrophage activation. Here, PF4 is linked to systemic sclerosis.