The mitogen-activated protein kinase (MAPK) pathway has been reported to be involved in the transcription of TGF-β, and p38 is involved in the phosphorylation of Smad2/3 in keloid fibroblasts, whereas extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) promote translocation of Smad2/3/4 complex, which in turn regulates the expression of related genes, such as plasminogen activator inhibitor-1 (PAI-1) [48]. The gene discussed is SMAD2; the disease is keloid.