In this context, it is reasonable to suppose that potential candidates will include a large array of mediators and signaling pathways that are known to be dysregulated in SSc and that have already been demonstrated to induce EndMT and/or Ly-EndMT, such as canonical and non-canonical TGFβ signaling, Notch, PPARγ, endothelin-1, and a variety of miRNAs [8,11]. The gene discussed is PPARG; the disease is systemic sclerosis.