In context, antisense oligonucleotide therapy (TPI ASM8), developed to suppress the expression of surface receptors CCR3 (C-C chemokine receptor type 3, binds eotaxin) and β chain (shared receptor for IL-5, IL-3 and granulocyte macrophage-colony stimulating factor, GM-CSF) [36], reduced sputum eosinophil counts by 46%; while a CCR3 antagonist was recently documented to show no effect of blood or sputum eosinophilia or to have any clinically improvement in moderate to severe asthmatics [37]. The gene discussed is CCL11; the disease is Increased total eosinophil count.