gd T cells develop in the thymus and are enriched in intraepithelial layer of intestine. The development and differentiation of gd T cells were previously thought to be dependent on their TCR usage, and V1 (Vd6.3^–Vg1.1⁺), V6 (Vd6.3⁺Vg1.1⁺) and V2 (Vg2⁺) gd T cells represented IFNg, IL-4 and IL17 producing subsets respectively. Here we show that, regardless of their TCRs, CD24^hi gd T cells are immature and CD24^low gd T cells expressed PLZF and differentiated into effector lineages expressing TBET (PLZF^low), GATA3 (PLZF^hi) and RORgt (PLZF^int). In the thymic medulla, these cells produced IFNg, IL-4 and IL17 respectively and transcription factors, rather than their TCR usage, determined the cytokine nature of gd T cells. In the gut, intraepithelial gd T cells were uniformly PLZF^– TBET⁺ expressing V5 (Vg5⁺) TCR, but derived from previously PLZF⁺ cells. The development of intraepithelial gd T cells were not influenced by intestinal microbiome, but their activation was influenced by food antigens, suggesting their potential regulatory role. Remarkably, CD24^low V5, V6 and V2 gd T cells shared transcriptional nature with NKT1, NKT2 and NKT17 cells respectively, indicating PLZF regulates effector differentiation of both iNKT and gd T cells.