Memory CD8⁺ T cells are critical for long-term immunity, but the genetic pathways governing their formation remain poorly defined. This study shows that the IL-10-IL-21-STAT3 pathway is critical for memory CD8⁺ T cell development after acute LCMV infection. In the absence of either interleukin-10 (IL-10) and IL-21 or STAT3, virus-specific CD8⁺ T cells retain terminal effector (TE) differentiation states and fail to mature into protective memory T cells that contain self-renewing central memory T cells. Expression of Eomes, BCL-6, Blimp-1, and SOCS3 was considerably reduced in STAT3-deficient memory CD8⁺ T cells, and BCL-6- or SOCS3-deficient CD8⁺ T cells also had perturbed memory cell development. Reduced SOCS3 expression rendered STAT3-deficient CD8⁺ T cells hyperresponsive to IL-12, suggesting that the STAT3-SOCS3 pathway helps to insulate memory precursor cells from inflammatory cytokines that drive TE differentiation. Thus, memory CD8⁺ T cell precursor maturation is an active process dependent on IL-10-IL-21-STAT3 signaling.