ADAM17 (a disintegrin and metalloproteinase domain 17) expressed on MDSCs directly cleaves the ectodomain of L-selectin (CD62L) on naive T cells to inhibit them homing to peripheral lymph nodes and tumor sites.111 Moreover, downregulation of CD44 and CD162 on T cells by M-MDSCs-derived NO can damage T cells extravasation and tissue infiltration.112 In addition, NO was also reported to decrease E-selectin expression on tumor vessels, thereby inhibiting T cells trafficking to tumor tissues.113. Here, ADAM17 is linked to neoplasm.