This mechanism of action (dual binding to CD38 and BCMA) may overcome malignant plasma cell escape mechanisms associated with low tumor antigenic expression inherent to myeloma as preclinical work has shown that ISB 2001 demonstrates improved anti-myeloma activity when compared to other BCMA- or CD38-directed targeted therapeutic either as single agent or in combination across different MM models (75). The gene discussed is TNFRSF17; the disease is Miyoshi myopathy.