TGF-β1 stimulation in CFs resulted in increased proliferation, increased collagen I and collagen III expression, and increased p38 and ERK1/2 phosphorylation (Xu et al., 2017), whereas inhibition of the activation of p38 kinase and ERK1/2 could effectively attenuate cardiac fibrosis (Tao et al., 2016). The gene discussed is TGFB1; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.