A subset of T cells, tissue-resident memory T cells, have attracted substantial attention in the last decade. These are non-recirculating memory T cells that persist long-term in epithelial tissues.41 They evolved to provide rapid protection against pathogens, but when aberrantly activated, contribute to immune-mediated diseases such as psoriasis.41 This aberrant activation can happen in response to autoantigens, such as those presented by HLA-C*06:02. Autoantigens implicated in psoriasis pathogenesis include the melanocyte antigen ADAMTSL5,42 the cathelicidin antimicrobial peptide LL37,43 and KRT17.44 The persistence of tissue-resident memory T cells in the skin can explain several features of psoriasis, including the sharp demarcation of involved skin from clinically healthy skin40 and the characteristic recurrence of psoriasis at previous sites of involvement.