WNK1, a Ser/Thr protein kinase, is widely expressed in many tissues. Its biological functions are largely unknown. Disruption of the WNK1 gene in mice leads to embryonic lethality at day 13, implicating a critical role of WNK1 in embryonic development. To investigate this potential function, we used antisense strategy to knock down the expression of WNK1 in a mouse neural progenitor cell line, C17.2. Down‐regulation of WNK1 in C17.2 cells greatly reduced cell growth. Addition of epidermal growth factor (EGF), a mitogen for C17.2 cells, had no effect on growth. The WNK1‐knockdown cells showed a flat and rounded morphology, characteristic of the immature and non‐differentiated phenotype of the progenitor cells; this was further demonstrated by immunostaining for the progenitor and neuronal markers. Migration of the WNK1‐knockdown C17.2 cells was reduced as tested in culture dishes or Matrigel‐covered chambers. Moreover, activation of extracellular signal‐regulated kinase (ERK1)/2 and ERK5 by EGF in the WNK1‐knockdown cells was suppressed. These results demonstrate a novel function of WNK1 in proliferation, migration, and differentiation of neural progenitor cells, likely by mechanisms involving activation of the mitogen‐activated protein (MAP) kinase ERK1/2 and/or ERK5 pathways.