In response to persistent viral infection, CD8 T cells progressively lose their effector function, in a differentiation process coined T cell “exhaustion”. While recent evidence indicates that the pool of exhausted cells is comprised of multiple heterogenous populations, including a progenitor subset that can bifurcate into terminally exhausted or cytolytic effector cells, the molecular circuits underpinning CD8 T cell differentiation during chronic infection remains unclear. Using scRNA-seq and flow cytometry, I look to uncouple these molecular pathways identifying novel genes that are key in this terminal bifurcation process.