Nonetheless, EMD and disease burden also compromise non-BCMA BsAbs, indicating sBCMA-independent mechanisms are relevant, such as a low effector-to-target ratio and impaired T-cell infiltration of large lesions (11, 109).The extramedullary tumor milieu may also hamper immunotherapeutic approaches since immune checkpoint molecules, immunosuppressive cytokines [i.e., transforming growth factor-beta (TGF-β), and interleukin-10 (IL-10)], and immunosuppressive cells hinder the anti-tumor immune response and limit immune effector cell entry to these sites (110–112). Here, IL10 is linked to neoplasm.