As activation of p53 signaling is believed to play a role in the anti-MM effects of CARM1 inhibition, and the CARM1 inhibitory activity of IMiD-based 074 is functionally preserved, it is possible that for patients with TP53 abnormalities, maximum clinical benefit may be achieved by combining 074 with p53-targeting agents and/or other proapoptotic agents capable of overriding drug resistance due to mutated p53.7 The gene discussed is TP53; the disease is Miyoshi myopathy.