Contrasting with its oncogenic role in solid tumors (e.g., as a lung cancer biomarker) (Sánchez-Tena et al., 2016), HECT E3 ligase HERC4 demonstrates tumor-suppressive activity in MM through two distinct mechanisms: one way is to mediate the polyubiquitination and proteasomal degradation of c-Maf to specifically reduce c-Maf protein level (Zhang et al., 2016). The gene discussed is MAF; the disease is Miyoshi myopathy.