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Critically, integrating genomic and molecular data has uncovered fundamental mechanisms of patient heterogeneity, such as the discovery that a diurnal BMAL1-HIF2A complex regulates myocardial vulnerability to injury, providing a molecular rationale for the long-observed circadian patterns of MI severity and opening the door to chronopharmacologytiming interventions for maximum efficacy (Ruan et al., 2025)

RSL3 treatment reduced the tumor area in both the H1299 and H23 cell xenografts (Fig

The role of plasma cytokine levels, CRP and Selenoprotein S gene variation in OA

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