This conclusion is in agreement with previous observations showing that IL‐6 trans‐signaling and TGF‐β are critical for the development and activation of Th17 cells (Dominitzki et al, 2007; Korn et al, 2009; Jones et al, 2010), and that neutralization of IL‐6 signaling functioning downstream of IL‐17A efficiently reduces the psoriasis‐like pathogenesis, including infiltration of effector T cells, formation of neutrophil microabscesses, and acanthosis in the skin of IL‐17A‐overexpressing mice (Croxford et al, 2014). The gene discussed is IL17A; the disease is psoriasis.