In multiple myeloma, ADAR1 enhanced Alu-dependent editing and transcriptional activity of GLI1, a Hedgehog (Hh) signaling pathway transcriptional activator and self-renewal agonist, leading to an R701G amino acid change, which stabilized GLI1 transcriptional activity by preventing the binding of a critical Hh signaling pathway negative regulator, and resulted in promotion of immunomodulatory drug resistance.38 Importantly, inactivation of ADAR1 reduced the resistance to blockade and overcame the resistance to immunotherapy.39 The gene discussed is GLI1; the disease is AL amyloidosis.