Invariant natural killer T (iNKT) cells are innate-like T cells that rapidly produce cytokines that impact anti-microbial immune responses, asthma, and autoimmunity. These cells acquire multiple effector fates during their thymic development that parallel those of CD4⁺ T helper cells and the recently identified Innate Lymphoid Cells (ILCs). The number of Th2-type effector iNKT cells (NKT2) is variable in different strains of mice and their number impacts CD8 T cell, dendritic cell, and B cell function. We have recently established that the E/ID protein pathway has multiple roles during iNKT cell development and it severely impacts iNKT cell specification and iNKT cell effector polarization. We show here evidence that the ID function is, in part, mediated by the transcription factor Lymphoid Enhancer Factor 1 (LEF1), a member of the TCF/LEF family of High Mobility Group (HMG) proteins. In addition to regulating the intrathymic proliferative phase of iNKT cells, we show that LEF1 can non-redundantly control development of NKT2 cells, through direct regulation of the Gata3 gene. Importantly, ectopic expression of LEF1 in iNKT cells results in an increase of NKT2 cell frequency. Therefore, we have identified the E/ID and LEF1/TCF1 pathways as central co-regulators of iNKT effector subset differentiation.