The identified variants in ABCG2, SLC29A1, and ABCC4 may collectively contribute to an increased risk of febuxostat-induced agranulocytosis by altering the drug’s pharmacokinetics and pharmacodynamics through the following possible mechanisms: altering drug transport and clearance inducing higher systemic and intracellular levels of febuxostat; increasing exposure to toxic metabolites, leading to bone marrow suppression and disrupting normal cellular processes, which affect neutrophil production and survival. Here, SLC29A1 is linked to Absence of circulating granulocytes.