A genome-wide association study (GWAS) conducted on a European population by Wadelius M et al. revealed that those with genetic variants in HLAB*08:01 and HLAA*31:01 had an increased susceptibility to developing sulfasalazine-induced agranulocytosis.4 In addition, idiosyncratic skin and lupus-like reactions have been attributed to slow NAT2 Acetylators. The gene discussed is HLA-A; the disease is Absence of circulating granulocytes.