Consistent with our findings, Lee et al. have demonstrated that the presence of DM enhances the systemic pro-inflammatory milieu in AS patients by showing increased expression of various markers such as E-selectin, IL-1 receptor, and intercellular adhesion molecule 2, all of which contribute to the escalation of myocardial fibrosis, diastolic dysfunction, and poorer clinical outcomes [46]. This evidence concerns the gene ICAM2 and diabetes mellitus.