In this work, we describe the ability of BETi to upregulate the NKG2DL MICA (cell surface, messenger RNA (mRNA) expression and promoter activity) in MM cells, with little or no effects on the expression of other NKG2DL (e.g., MICB) and the DNAM-1L PVR/CD155. The gene discussed is MICB; the disease is Miyoshi myopathy.