In skin biopsies of patients with systemic sclerosis with calcinosis, the expression of hypoxia-related glucose transporter molecule 1 increased,[4] and the level of vascular endothelial growth factor, an effective angiogenic factor induced by hypoxia.[5] The imbalance between hypoxia-induced angiogenic factors (such as vascular endothelial growth factor) and antiangiogenic factors (such as angiostatin) is common in the pathogenesis of tissue fibrosis and calcinosis cutis.[4–6]. Here, PLG is linked to calcinosis.