MAF and Miyoshi myopathy: Based on these findings, coupled with the clinical observation that MAF translocated MM shows innate resistance to proteasome inhibition, we speculate that increased activity of the hexosamine pathway can stabilize MAF proteins, a function that could be important regardless of overexpression through translocation, and that activity of the HBP through glycolytic intermediates is associated with stabilization of NRF1 and increased mitochondrial fitness.