Of note, in recent studies the c-MYC proto-oncogene, which is de-regulated in about 30–50% of patients with advanced MM and is associated with a poor prognosis [41], has been shown to promote either constitutive HIF-1α protein activation, or aberrant VEGF production by plasmacells (PCs) and angiogenesis under normoxic conditions [27, 41, 42]. This evidence concerns the gene VEGFA and Miyoshi myopathy.