Stimulation of JNK causes a sequential transcriptional activation that promotes an early ROS-independent stimulation of fibrotic markers such as CTGF (Figure 5A and Figure 6D) and, at later time points, the establishment of a NOX-4-dependent long-term α-SMA expression, which generates a pro-fibrotic microenvironment that promotes cancer progression. The gene discussed is ACTA1; the disease is cancer.