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. This evidence concerns the gene ADAM9 and melanoma.