ADAMTSL5 (ADAMTS-like 5) is a secreted glycoprotein with emerging roles in both extracellular matrix organization and immune-mediated disease. In normal physiology, ADAMTSL5 likely modulates fibrillin microfibrils in the extracellular matrix through microfibril binding activity. However, ADAMTSL5 has been identified as a key psoriasis autoantigen that is significantly upregulated in active psoriatic lesions, where it localizes with keratinocytes, dendritic cells, and other leukocytes 1. ADAMTSL5-reactive T cells contribute to pathogenic responses in psoriatic patients, and autoreactivity to both LL37 and ADAMTSL5 is associated with reduced clinical response to risankizumab therapy and altered T-cell modulation 23. ADAMTSL5 expression is elevated following anti-PD-1 checkpoint inhibitor therapy and correlates with psoriasis-like manifestations 4. Beyond dermatology, ADAMTSL5 functions as a master regulator of oncogenic signaling in hepatocellular carcinoma, maintaining receptor tyrosine kinase activation and drug resistance; ADAMTSL5 depletion sensitizes HCC cells to sorafenib, lenvatinib, and regorafenib 5. Additionally, in gastric cancer, ADAMTSL5 expression is suppressed by the circPFKP/miR-644 regulatory pathway, suggesting a tumor-suppressive role 6. Elevated anti-ADAMTSL5 antibodies in psoriatic serum support diagnostic potential 7.