Given that CD80 and CD86 engagement with CD28 on CD8 T cells amplifies TCR/CD3 signaling, these data indicate that inhibition of the PD1/PD-L1 pathway with co-targeting sMIC could potentially facilitate a more vigorous CD28-mediated co-stimulatory signal delivered to antigen-specific CD8 T cells for the sustained anti-tumor activity. Here, CD86 is linked to neoplasm.