Across atopic dermatitis (AD), prurigo nodularis (PN), psoriasis, cutaneous T-cell lymphoma (CTCL), dermatomyositis, and primary localized cutaneous amyloidosis (PLCA), both IL-31 and OSM contribute to chronic itch through overlapping pathways, including shared receptor architecture and activation of JAK1-STAT3 signaling. This evidence concerns the gene IL31 and primary cutaneous T-cell non-Hodgkin lymphoma.