Abstract The transcription factor PLZF is required to drive lineage diversification of would-be conventional T cells into the natural killer T cell fate. However, the molecular machinery linking extracellular signaling to this fate choice is unknown. Recently, the early growth response 2 (Egr2) transcription factor, a calcineurin-dependent lineage resolution factor, was found to be important for NKT development. Here, we utilize an Egr2/IRES-GFP transgenic mouse model to show that Egr2 is uniquely induced immediately after TCR engagement in NKT cells. Competitive bone marrow chimeras with T cell conditional knockout mice indicate that Egr2 is required for both stage zero to stage 1, and stage 2 to stage 3 transitions of NKT development. Importantly, Egr1/Egr2 double deficient, stage 1 arrested NKT cells fail to express PLZF, in striking contrast to wild type stage 1 NKTs. Gel shift analysis shows in vitro translated Egr2 protein binds to a conserved site within the zbtb16 (PLZF) promoter. ChIP-seq of Egr2-bound chromatin from thymic NKTs confirmed in vivo binding of the zbtb16 promoter. Finally, we show that strong TCR signals are important for Egr2 induction in NKT cells. We propose that Egr2 links the NKT TCR signal with resolution of a mixed lineage state, driving PLZF expression in addition to other critical NKT lineage properties. We also suggest other receptor-dependent cell fates may be controlled by similar induction of resolution factors.