FCGR3A and neoplasm: Given that concurrent activation of FcγRIIIa and NKG2D enhances immune cell activation (Fig. 5A), we hypothesized that 23ME-01473, an anti-ULBP6/2/5 with an effector-enhanced (afucosylated) Fc domain (53), could capitalize on the presence of ULBP6/2/5 on the surface of tumor cells to activate FcγRIIIa and induce ADCC while concurrently neutralizing sULBP6 to release NKG2D to bind activating surface NKG2DLs.