While CAR‐T‐cell therapy has become an essential treatment for RRMM, addressing CAR‐T‐cell exhaustion remains a significant challenge.[2, 3] Building on our findings that the CD161–CLEC2D interaction induces CD8+ BM‐TRM dysfunction and promotes MM progression, we next determined whether CD161 is expressed on CAR‐T cells in RRMM patients and whether it contributes to their functional exhaustion. This evidence concerns the gene KLRB1 and Miyoshi myopathy.