After acute kidney injury (AKI) attacks, the c-Jun NH2-terminal kinase (JNK) signal is activated in tubular epithelial cells to enhance the expression of typical mesenchymal markers (e.g., e-cadherin, α-smooth muscle actin) and to upregulate profibrogenic factors (mainly transforming growth factor (TGF)-β and connective tissue growth factor (CTGF)) [17]. The gene discussed is TGFB1; the disease is acute kidney injury.