The receptor Flt3 and its ligand Flt3L are both critical for dendritic cell (DC) development, but DC deficiency is more severe in Flt3l−/− mice than in Flt3−/− mice. This has led to speculation that Flt3L binds to another receptor that also supports DC development. However, we found that Flt3L administration does not generate DCs in Flt3−/− mice, arguing against a second receptor. Instead, Flt3−/− DC progenitors matured in response to macrophage colony–stimulating factor (M-CSF) or stem cell factor, and deletion of Csf1r in Flt3−/− mice further reduced DC development, indicating that these cytokines could compensate for Flt3. Surprisingly, Flt3−/− DC progenitors displayed enhanced M-CSF signaling, suggesting that loss of Flt3 increased responsiveness to other cytokines. In agreement, deletion of Flt3 in Flt3l−/− mice paradoxically rescued their severe DC deficiency. Thus, multiple cytokines can support DC development, and the discrepancy between Flt3−/− and Flt3l−/− mice results from the increased sensitivity of Flt3−/− progenitors to these cytokines.