This study investigated the effects of selexipag and ACT-333679 in reducing the activity of cultured skin SSc fibroblasts and their ECM protein overproduction, through the ability to interfere with the activation of those intracellular signaling transduction molecules involved in the regulation and progression of fibrosis, primarily MAPK family members (i.e. extracellular signal-regulated kinases 1 and 2 (Erk1/2)) and protein kinase B (PKB or Akt). The gene discussed is MAPK3; the disease is systemic sclerosis.