While a recent meta-analysis by Liu et al. [16] reported that long-term use of GLP-1 analogs was associated with increased risk of DVT in general population with T2DM or other metabolic syndromes, contrasting with our findings, our study focused on a distinct population with RA who carry chronic systemic inflammation, and have unique pathophysiological mechanisms including endothelial dysfunction and upregulated inflammatory cytokines which are known to increase thrombotic risk. The gene discussed is GLP1R; the disease is inflammation.