SLAMF7 serves as a self‐ligand and has a unique co‐stimulatory function in NK cells.[26] As a clinically approved therapy target, SLAMF7 on the MM cell surface directly binds to SLAMF7 on NK cell or its MoAbs followed by binds to FcgRIIIa/CD16 on NK cells, resulting in NK cell‐mediated MM cell killing.[24c] Elevated surface SLAMF7 by CAV1 knockdown, even in RPMI8226 cells expressing low endogenous levels of SLAMF7, would promote the SLAMF7‐mediated interaction between NK and MM cells and thus enhance cytotoxicity against MM cells. Here, FCGR3A is linked to Miyoshi myopathy.