PDK1 and Miyoshi myopathy: In MM, it was demonstrated that PDK1 is expressed and active in all eleven MM-derived cell lines, regardless of the type of cytogenetic abnormality or the status of upstream signaling molecules, and that genetic or pharmacological (BX-912) inhibition of PDK1 caused the growth inhibition and the induction of apoptosis, and augmented the in vitro cytotoxic effects of antimyeloma agents such as melphalan, etoposide, or bortezomib [17].