This includes the steering of important pathophysiological processes in RA, such as ECM formation and fibrosis induction (guided by SMAD3; [62]), proliferation, cell survival, and inflammation (driven by RelA; [66]), as well as differentiation or dedifferentiation (controlled by SNAI2 [67] or GLI2 [68]). Here, GLI2 is linked to rheumatoid arthritis.