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). The gene discussed is ITGA4; the disease is Miyoshi myopathy.