There are two central themes in my lab: 1) My research has found that βII spectrin associates with ankyrin- B and represents an integrative node for assembly of the cardiac junctional dyad. My lab has discovered a novel mutation in the human ankyrin-B gene that disrupts the ankyrin-B/βII spectrin interaction leading to severe human arrhythmia phenotypes. My lab has observed aberrant βII spectrin regulation in multiple forms of human heart failure and arrhythmia and accelerated heart failure phenotypes in βII spectrin-deficient cardiac-specific mice. 2) As a Heart failure (HF)-transplant cardiologist, I routinely see patients who have had increased cancer-free survival due to anti-cancer treatment, however, go on to develop cardiotoxic side effects including overt HF. Thus, my goal is to generate new mechanistic data using in vitro and in vivo models to determine the underlying cardiotoxic pathways anti-cancer therapy has on the heart.  My mission is to translate these findings to other disease states and pathways using novel and cutting-edge methods and technologies, including inducible pluripotent stem cell cardiomyocytes and cardiovascular optogenetics.  My lab has been continuously supported by NIH funding since 2014 (Current funding as Primary PI: NIH R01HL160590).