Furthermore, Nintedanib exposure upregulated the cyclin-dependent kinase inhibitors such as CDKN1 and 2 that act like negative regulators of cell cycle progression alongside growth arrest and DNA damage-inducible 45 (GADD45), a tumor suppressor known to play a role in mediating the anti-cancer activity of several chemotherapeutic drugs29,30. The gene discussed is CDK1; the disease is cancer.