In parallel, inflammatory–clock crosstalk (NF-κB–mediated suppression of BMAL1/PER2) blunts diurnal vascular reactivity and contributes to endothelial dysfunction (Curtis et al., 2014; Shen et al., 2021), while endothelial nitric oxide synthase (eNOS) normally exhibits a circadian rhythm promoting daytime vasodilation and nocturnal pressure decline [91–94]. The gene discussed is NFKB1; the disease is endothelial dysfunction.