Moreover, they propose that hY4-induced responses were dependent on endosomal TLR7 and consistent with this hypothesis, they found that upon treatment with CLL-derived sEVs or hY4 the pharmacological inactivation of TRL7 significantly reduced cytokine release and PD-L1 expression in monocytes in vitro and attenuated CLL development in vivo. Here, CD274 is linked to B-cell chronic lymphocytic leukemia.