For example, GWAS has: (i) linked IL6R variants to C-reactive protein (CRP) levels and motivated trials of tocilizumab and other IL6R antagonists in rheumatoid arthritis and coronary disease [8]; (ii) highlighted CYP2C19 polymorphisms affecting clopidogrel metabolism and led to genotype-guided antiplatelet therapy recommendations [9]; (iii) identified lipoprotein(a) variants that informed the development of antisense therapies targeting apolipoprotein(a) [10]. Here, CRP is linked to rheumatoid arthritis.