A growing body of literature indicates that relapse is initiated by tissue-resident memory T (TRM) cells that are poised to produce IL-17A and IL-22 in resolving lesions.37,38,39,40,41,42 CD28 expression is highly variable in TRM cells and not present on most CD8+ TRM cells in healthy skin.43 Therefore, it is plausible that psoriasis relapse is triggered by CD28-independent, compensatory activation of IL-17A-producing CD8+ TRM cells that reignite the psoriasis molecular signature. The gene discussed is IL17A; the disease is psoriasis.