The depletion of BM CD8+ TRM and increased expression of inhibitory receptors, such as PD‐1 and T cell immune receptor with Ig and ITIM domains (TIGIT), correlate with weakened immune surveillance in MM patients.[6] However, single‐agent blockade targeting these pathways fails to effectively rescue TRM function.[6b]. The gene discussed is CD8A; the disease is Miyoshi myopathy.