However, treatment with CoCl2, a chemical approach widely used to mimic hypoxia, failed to induce either HIF‐1β expression or NF‐κB activation in MM cells, while resulted in HIF‐1α accumulation (Figure S3B), presumably due to blockade of its degradation.13, 38 These results indicate that hypoxia (eg, low O2 concentration or the chemical mimetic lactic acid, but not CoCl2) is able to induce ARNT/HIF‐1β expression and NF‐κB activation in MM cells, suggesting a potential role of HIF‐1β and its relationship with NF‐κB in hypoxic MM microenvironment. The gene discussed is HIF1A; the disease is Miyoshi myopathy.