In MM, γδ T cells are activated by non-peptide antigens and stress-induced ligands, exhibiting cytotoxic activity by killing MM cells via perforin, granzyme, and death receptor pathways, and recognizing stress-induced ligands such as MICA/B and ULBP1-4 via the NKG2D receptor [286–289]. Here, PRF1 is linked to Miyoshi myopathy.