We are investigating the developmental origins of alterations in striatal interneurons observed in brain of patients diagnosed with Tourette’s Syndrome using organoid models cultured from patient-derived induced pluripotent stem cells. Here we provide a first characterization of organoids differentiated using a new protocol aimed to induce ventral forebrain fates in 7 iPSC lines from neurotypical adults. During neural induction with dual SMAD inhibition, patterning was carried out over 5 days using the Wnt-antagonist XAV939 alone in our standard dorsal forebrain protocol, and in combination with SHH-agonist purmorphamine in the ventral forebrain protocol. RNA sequencing after 30 days of terminal differentiation revealed 1418 differentially expressed genes. In ventral as compared to dorsal forebrain organoid preparations, Hoxb cluster genes, NKX2.1, NKX2.2, NKX6.2, SHH, and FOXA1 were among the strongly upregulated genes, whereas EMX1, TBR1, NEUROD6, and EOMES were among strongly downregulated genes (log2 fold change>5). While immunostaining revealed the presence of NKX2.1 positive cells with both protocols, somatostatin (SST) and Choline acetyltransferase (ChAT) positive interneurons were consistently more abundant in the ventral forebrain condition (excepting one line) and were less abundant or absent in the dorsal forebrain protocol. Taken together, while our standard dorsal forebrain protocol appears to yield some inhibitory neurons, these neurons are more abundant in our ventral forebrain organoids along with cell types of more posterior fates. Thus, our new protocol promises to be useful for the investigation of movement disorders arising from potential dysfunction of basal ganglia and adjacent regions of the diencephalon and midbrain.