As in the case of ADAM8, recent studies have shown that both ADAM10 and ADAM17 may also cleave PD-L1, with their expression and activation correlating with soluble PD-L1 levels, a mechanism that can suppress anti-tumour immunity by promoting apoptosis in CD8+ T cells, particularly in triple-negative breast cancer (TNBC) [11,94,116]. This evidence concerns the gene ADAM8 and neoplasm.