In spite of this, clinical trials studying monotherapy with PD1/PDL1 inhibitors have yielded lackluster results, and this is likely due to the highly dysfunctional MM T cells, which coexpress T-cell immunoglobulin mucin-3 (TIM3) and lymphocyte-activation gene 3 (LAG3), and a combined blockade of multiple checkpoint pathways may be needed [116,117,120]. The gene discussed is PDCD1; the disease is Miyoshi myopathy.