Invariant Natural Killer T (iNKT) cells play a central role in several immune responses in diverse biological contexts ranging from autoimmunity, injury and infections to pregnancy and cancer. Three major phenotypically and functionally distinct iNKT cell subpopulations, each with a propensity to traffic to different tissues and to secrete different cytokines upon activation, have been identified. These fate assignments are already evident in the thymus, suggesting that they are conferred upon iNKT cells during selection, although the cues that direct these decisions remain poorly understood. Since the strength of signal propagated through the T cell antigen receptor (TCR) has been demonstrated to influence T cell fate both in the thymus and periphery, we explored the contribution of the TCR to iNKT subset diversification. Here, we show that in wildtype mice, the avidity of the iNKT TCR correlates with iNKT cell subsets and the differential expression of various markers reflecting strength of signaling during selection. Interestingly, the TCRβ chains utilized by the iNKT cells are unique to each iNKT cell subset. Additionally, altering the signal transduced through the TCR during selection, either through the use of a fixed TCRβ chain or a mouse containing a hypomorphic TCR signaling kinase (Zap70), dramatically affected the ability of iNKT cells to properly diversify, exemplified by the preferential reduction of the PLZF^hi and RORγt⁺ subsets. These data provide support for the idea that the TCR signaling event perceived by each iNKT precursor during selection serves as a branching point for the different cells, each of which then follows a distinct developmental program culminating in differentiation into one of the three lineages