Depletion of Ca2+ influx channels, including TRPM7, ORAI1, and STIM1, in human-derived MM cells causes hyper-O-GlcNAcylation and subsequent ubiquitin-proteasome mediated degradation of ITGA4 and ITGB7, leading to their decreased expression and consequential reduction in MM cell motility and dissemination (Fig. 8C). This evidence concerns the gene STIM1 and Miyoshi myopathy.