In contrast, GM-CSF blockade with mavrilimumab may address the pathogenic mechanisms of GCA more comprehensively via its demonstrated suppressive effects on macrophages, CD4+ Th17 cells, and CD4+ Th1 cells, including downregulation of IFNγ expression.22 23 However, further mechanistic research linked to clinical outcomes is needed before firm conclusions can be drawn. The gene discussed is CD4; the disease is temporal arteritis.