Recent research has focused on identifying the specific inflammatory pathways involved in the progression of NCVs, notably the NLRP3 inflammasome, a crucial component of the innate immune response.[18] Activation of the NLRP3 inflammasome results in the production of IL-1β, perpetuating inflammation and influencing smooth muscle cell proliferation and migration, contributing to plaque formation in NCVs.[24] Additionally, systemic inflammatory markers such as C-reactive protein (CRP) correlate with the extent of atherosclerosis in NCVs and serve as potential prognostic indicators. The gene discussed is CRP; the disease is atherosclerosis.