More recently, the occurrence of EndMT in SSc has been related to elevated levels of oncostatin M, a member of the IL-6 family, and the inflammatory lipid mediator leukotriene B4, with the former being able to induce myofibroblast-like morphologic changes in healthy dermal microvascular endothelial cells, and the latter to promote the myofibroblast transition in endothelial cells through the activation of the phosphatidylinositol 3-kinase/protein kinase B (AKT)/mammalian target of the rapamycin (mTOR) pathway [50,51]. Here, MTOR is linked to systemic sclerosis.