Due to cellular IAPs’ simultaneous role in regulating NFκB signaling, treatment with IAP antagonists sensitizes tumor cells to apoptotic signals while increasing alternative NFκB signaling in T cells and the tumor microenvironment in promising ways that may support immunotherapy for MM (Chesi et al. 2016, Gu et al. 2021, Roehle et al. 2021). The gene discussed is NFKB1; the disease is Miyoshi myopathy.