Our findings of reduced motif activity and expression of RUNX2 in VSMCs from MAPK14 KO mice further support the regulatory role of MAPK14 in RUNX2 transactivation of downstream genes and, consequently, vascular calcification.66 Given the causative role of vascular calcification in aortic aneurysm progression,67–69 it will be essential to investigate whether MAPK14 loss in VSMCs reduces aortic calcification in vivo, providing further insight into the MAPK14/RUNX2 axis as a therapeutic target for aortic aneurysm. The gene discussed is RUNX2; the disease is aortic aneurysm.