Psoriasis, characterized by chronic inflammation and keratinocyte proliferation, involves intricate autoinflammatory and T-cell-mediated autoimmune responses.33 Autoinflammatory pathways lead to increased infiltration of effectors such as plasmacytoid dendritic cells (pDCs), myeloid dendritic cells (CD11c+ mDCs), neutrophils and natural killer (NK) cells, and antimicrobial peptides (AMPs).34–37 The downstream effects of these increased effectors lead to activated immune pathways, eventually increasing keratinocyte proliferation and sustained inflammation. The gene discussed is ADSL; the disease is psoriasis.