Interestingly, the initial results from the first-in-human phase I study of DTP3 in patients with relapsed/refractory MM confirmed the clinical capacity of this novel anticancer therapeutic to induce a cancer-selective pharmacodynamic response, triggering JNK signalling and apoptosis in MM, but not normal cells of patients, whilst producing no signs of toxicity and no adverse effects [28], thus providing clinical proof-of-concept for the novel approach to therapeutically block oncogenic NF-κB survival signalling. The gene discussed is NFKB1; the disease is Miyoshi myopathy.