Erin Mulkearns-Hubert's overall research goal is to understand the molecular events underlying human disease to propel therapeutic development. Glioblastoma remains one of the most treatment-refractory cancers, a characteristic that is at least in part driven by the presence of therapeutically resistant cancer stem cells. Her previous laboratory experiences have provided her with an extensive background in basic cell biology coupled with work on a variety of disease states. Her postdoctoral fellowship in the laboratory of Justin Lathia allowed her to combine her solid foundation in mechanistic biology with her interest in the pathogenesis of disease to develop next-generation targeted therapies and improve patient outcomes. She has a long-standing interest in the effect of the tumor microenvironment on cancer stem cells, including how cancer stem cells use transmembrane proteins to communicate with one another and with other types of cells in the tumor microenvironment. Mulkearns-Hubert was part of a team that discovered the presence of functional gap junctions in glioblastoma cancer stem cells and then identified a requirement for connexin 46, a gap junction protein, in the survival of and tumor formation by these cells. She subsequently led studies that mapped the essential function of connexin 46 to its role in cell-cell communication and began preclinical development of a specific connexin 46 inhibitor that we identified through a drug-repurposing approach. She also played a key role in work identifying a complex containing connexin 26, focal adhesion kinase, and the pluripotency transcription factor NANOG that drives cancer stem cells in triple-negative breast cancer and led studies developing a cell-penetrating peptide to target this complex.