Consistent with the aforementioned in vitro observations, the notion that adipose tissue-resident stem/progenitor cells may contribute to the accumulation of fibrogenic myofibroblasts and the development of skin sclerosis is substantiated by cell fate mapping studies in the most widely used preclinical model of SSc, namely mice with bleomycin-induced scleroderma, where the majority of pathogenic myofibroblasts were found to arise from adiponectin-positive progenitors resident in the dermal white adipose tissue [14,15]. This evidence concerns the gene ADIPOQ and scleroderma.