In support of this, direct contact with BMSC was only very recently shown to counteract doxorubicin and 4-hydroxycyclophosphamide induced hypermethylation of H3K27 in MM cells via phosphorylation-mediated inactivation of EZH2, leading to the sustained expression of anti-apoptotic genes (including IGF1, B cell CLL/lymphoma 2 (BCL2), and hypoxia inducible factor 1α subunit (HIF1A)) and hence cell adhesion–mediated drug resistance (CAM-DR). Here, IGF1 is linked to Miyoshi myopathy.