His research focuses on the mechanistic understanding and therapeutic targeting of the resistance by MM or other neoplasias against pharmacological and immune therapies. His studies established that inhibiting BET bromodomain proteins suppresses the function and expression of the oncoprotein c-Myc, leading to major interest for BET bromodomain inhibition in MM and beyond. His preclinical work informed the development of several regimens which are now standard-of-care for MM treatment, contributed to the improved survival of MM patients in the last decade and are a "backbone" for combination with newer therapies, e.g., monoclonal antibodies. His studies characterized how nonmalignant cells in the tumor microenvironment can protect MM or other neoplasias from diverse drugs or immune therapies; and developed preclinical models to simulate more accurately these interactions. Using CRISPR-based functional genomics, the Mitsiades lab dissected both genomic and non-genomic mechanisms of tumor cells’ persistence and resistance against pharmacological agents or immune effector cells, e.g., NK cells. Their CRISPR studies also identified a large collection of genes that are preferentially more important for MM than the large majority of other neoplasias, leading to a large new compendium of promising and previously understudied therapeutic targets for MM. Dr. Mitsiades is Senior Editor of Clinical Cancer Research; Vice-Chair for Translational Science in the MM Committee of the Alliance for Clinical Trials in Oncology. He received the 2019 Ken Anderson Award of the International Myeloma Society and was inducted into the American Society of Clinical Investigation (2021)