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Dr. Drumm’s doctoral degree was earned in the laboratory of Francis Collins, M.D., Ph.D., with whom he was a co-discoverer of the gene that causes cystic fibrosis (CF). Dr. Drumm continues to work on CF and joined the faculty at �ǿմ�ý in 1992 as an assistant professor in the Departments of Pediatrics and Genetics and Genome Sciences and currently holds the rank of professor in both departments.

His work in the early 1990s showed that CF cells could be “corrected” by introduction of a normal copy of the CF gene and laid the groundwork for studies in CF gene therapy.  He also demonstrated that the most common mutation found in CF was not entirely inactive and could be manipulated to exhibit ion channel activity.  Based on that observation, he pioneered the search for drugs that could correct the underlying channel defect in CF as a therapeutic approach.  He has authored over 100 peer-reviewed manuscripts and several book chapters on cystic fibrosis and holds three patents relevant to the disease as well.  

In 2007, Dr. Drumm was appointed as Director of Basic Research of the Willard A. Bernbaum Cystic Fibrosis Research Center.  His research program continues to focus on the genetics of CF, but he also utilizes mouse genetics to better understand the disease and explore treatment strategies. 

Because of the successes in cystic fibrosis, Dr. Drumm brought together faculty from across the �ǿմ�ý campus in 2015 to form The Research Institute for Children’s Health.  This institute was launched to implement laboratory-to-clinic research programs for other rare, genetic disorders, patterned after the CF approach.  Dr. Drumm currently serves as the Institute’s director.  

His current research in CF focuses on the unmet needs for the disease, such as therapies that would serve patients for whom CFTR modulators are not effective.  He has active programs to understand altered metabolism in CF and how genes that modify CF disease severity convey their effects and is pursuing new technologies in gene editing to determine if the CF gene can be repaired in a clinically significant way.