GWAS conducted across diverse ancestries repeatedly mapped blood pressure variation to vascular calcium dynamics (ATP2B1 and CACN* loci), renal tubular transport mechanisms (UMOD and SLC4A7), renin-angiotensin-aldosterone system-related steroidogenesis (CYP17A1 and CYP11B2), and immune remodeling pathways (SH2B3), with several loci demonstrating sex- or ancestry-specific modulation and enrichment in resistant-hypertension cohorts, particularly within calcium-handling and steroidogenic pathways. This evidence concerns the gene UMOD and hypertensive disorder.