ADAM9 and glioblastoma: ADAM17‐mediated shedding of TNFR1 in hepatocytes suppresses proapoptotic signaling during hepatic stress,[47] and the increased level of sTNFR1 secreted by ADAM9‐null fibroblasts inhibits apoptosis of melanoma cells.[48] In the clinical context, sTNFR1 levels are elevated in patients with glioblastoma and endometrial cancer.[49, 50] In accordance with the mechanistic findings revealed in this study, the level of sTNFR1 progressively increases from non‐HCC individuals to patients with early stage HCC to patients with late stage HCC.