To elucidate whether the protective effect of lactate was mediated by metabolic activity of lactate or through the activation of GPR81 signalling, NCI‐H929 cells were cultured in medium supplemented with 20% sera from different MM patients (n = 10) and treated with BTZ or CFZ alone or in combination with AZD3965, a selective inhibitor of MCT1, or 3‐OBA, an antagonist of GPR81. This evidence concerns the gene HCAR1 and Miyoshi myopathy.