During my postdoctoral training, I uncovered that B-lymphoid transcription factors restrict glucose uptake and energy supply to set low thresholds for negative selection of autoreactive and transformed B-cells. As a research staff at City of Hope, I developed a new therapeutic concept based on pharmacological reactivation of signaling pathways that oppose the principal oncogenic driver and that are silenced in full-blown leukemia. Reactivation of these pathways proved as an unexpected strategy to overcome drug resistance. As a research scientist at Yale University, I investigated the mechanistic basis of the distribution and frequency of RAS-pathway mutations in B-cell malignancies to identify disease-specific vulnerabilities for therapeutic targeting. Currently, I am an Assistant Staff at the Cleveland Clinic. I am also a Cleveland Clinic Catalyst Grant recipient and a Case Comprehensive Cancer Center Pilot awardee. My research program focuses on (1) understanding how crosstalk between oncogenic signaling pathways can influence malignant transformation, and (2) investigating how metabolic status evolves during disease progression in B-cell leukemia and lymphoma. Given that development of drug resistance and relapse remains a critical challenge in the treatment of patients with B-cell leukemia and lymphoma, the goal of my research is to identify new therapeutic targets to improve precision medicine.