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 “chronopharmacology”—timing interventions for maximum efficacy (Ruan et al., 2025). Here, BMAL1 is linked to myocardial infarction.