Dr. Randak’s research, on the structural basis of CFTR gating and its dependence on the activity of adenylate kinase is shifting the current paradigm of how CFTR functions in vivo. His laboratory showed that the adenylate kinase inhibitor Ap5A potentiates activity of the F508del CFTR channel by interacting with CFTR residue Q1291. Using transgenic mice, he is evaluating the Q1291F CFTR mutant for the ability to rescue the intestinal phenotype of CFTR knockout mice and to reduce cholera toxin-induced loss of intestinal fluids. Dr. Randak was a recipient of the Harry Shwachman CF Clinical Investigator award and of an R01 grant.