What is more important, IL‐17 mediates inflammatory reactions via p38/c‐Fos, and JNK/c‐Jun activation was proved in an AP‐1‐dependent manner (including FOS),61 and blockade of interleukin 17 (IL‐17) or tumour necrosis factor alpha signalling in psoriasis following upregulation of FOXC1 was also demonstrated.62 The gene discussed is JUNB; the disease is psoriasis.