Taken together, our results in MM are consistent with previous reports on the role of GAL-3 as a key regulator of cell adhesion and inflammation in cancer [51–56]; it negatively regulates T-cell function and proliferation through interaction with LAG3, especially on CD8+ CTL, possibly by reducing the affinity of the T-cell receptor and its internalization. This evidence concerns the gene CD8A and Miyoshi myopathy.