It is notable that the three drugs that constitute the backbone of anti-MM therapy (proteasome inhibitors, Ikaros degraders, and glucocorticoids) (Durie et al. 2017) all effectively target MM superenhancers, which are essential in maintaining plasma cell identity (through IRF4 expression), primary oncogenic events (immunoglobin translocations), and progression events (MYC dysregulation) (Figure 2). The gene discussed is MYC; the disease is Miyoshi myopathy.