TNFRSF10B and melanoma: This enhanced therapeutic efficacy is likely attributable to a combinatorial approach involving direct ulixertinib‐mediated cytotoxicity, selective engagement of DR5 by the DR5 agonist scFv to trigger apoptotic signaling, and the presence of cytotoxic components within the EV lumen—an advantage absent in anti‐DR5 Ab conjugated LNPs.[27, 59] Supporting this data, prior studies have demonstrated that NK cell‐derived sEVs harbor cytotoxic proteins and intrinsic anti‐tumor properties, potentiating melanoma cell death and modulating the tumor microenvironment.[27]