Apigenin-mediated suppression of CK2 activity was accompanied by reduced phosphorylation of Cdc37 in MM cells, leading to the disassociation of Hsp90/Cdc37/client protein complexes and inducing the degradation of client kinase proteins including RIP1, Raf-1, Src, Cdk4, and AKT via the ubiquitin-proteasome pathway (Figure 4, 5, 6). Here, AKT1 is linked to Miyoshi myopathy.