Given that IL‐17 inhibitors target downstream effectors such as IL‐17A which influence keratinocytes directly without broad effects on upstream IL‐23 responsive cells such as Th17 and Tc17, patients with more complex disease may have psoriasis modulated by other effectors such as IL‐17F or IL‐22; a significant role for residual tissue resident memory cell‐17 or disease driven by upregulation of IL‐23 receptor, which are all targets of IL‐23 but not IL‐17A inhibition.20 This evidence concerns the gene IL23R and psoriasis.