ACTA1 and neoplasm: Interestingly, Hanley and coworkers could demonstrate that the underlying fibroblast-to-myofibroblast transdifferentiation was depending on intracellular reactive oxygen species generated by NOX4 and that pharmacological blockage of this enzyme caused decreased αSMA, inhibited positive myofibroblastic CAF formation, and slower tumor growth in both in vitro and in vivo models [55].