Dendritic cells (DCs) orchestrate immune activation and tolerance. As highly potent contributors to T cell priming, they represent an attractive target for therapeutic modulation. Unfortunately, their small and difficult-to-access natural progenitor pool presents difficulties for cell therapy development. Progenitor scarcity precludes in vivo reprogramming approaches and likewise limits scalable ex vivo manufacturing. Consequently, despite their extraordinary potency for T cell priming, DCs have yet to fulfill their therapeutic potential as anti-cancer cell therapies. Even today, many years after the first human trials of DC-based vaccines, these products are still generated from available monocyte-derived cells rather than rare bona fide DC progenitors, leading to suboptimal T cell priming and poor migration to lymphoid tissues. Developing robust systems for generating functional DCs at scale remains a critical unmet need in immunotherapy. We  have developed and defined a transcription factor-and-cytokine “3+3” framework that drives engineered myeloid progenitors toward cDC1 differentiation, providing a scalable platform for synthetic DC generation. Preliminary data demonstrates that conditionally arrested myeloid progenitors (Hoxb8 cells) can be reprogrammed into conventional DC type 1 (cDC1) cells in a cGMP-friendly manufacturing environment free of accessory feeder cells. Building on these discoveries, we aim to design optimal synthetic gene circuits to reprogram progenitors into specific DC states — particularly to maximize the yield of cross-presenting cDC1s, the critical, limiting cell type for anti-tumor immunity.