Notable findings include the upregulation of proteoglycan 4 (Prg4), known for its anti-inflammatory properties [41, 42], the downregulation of proteoglycan 2 (Prg2), a recognized tumour-suppressor [43], and the upregulation of cysteine-rich with EGF-like domain protein 2 (Creld2), which has implications for tumour progression via fibroblast reprogramming [44]. The gene discussed is CRELD2; the disease is neoplasm.