We studied the mechanism that the inhibition of proliferation by dexamethasone (DEX), which is added to odontoblast differentiation culture medium, is canceled for Intraflagellar transport (Ift) 88 knocked-down pre-odontoblastic KN3 cells (Ift88 is known to function in primary cilia formation and cell cycle control. ). As a result, while involvement of signal pathways via the primary cilia was not recognized, involvement of Ccn4 and Ccn5, which are canonical Wnt signal pathway related genes, was suspected. We then established and analyzed KN3 cells where Ccn4 and Ccn5 were overexpressed. However, it was revealed that Ccn4 and Ccn5 are not involved in the mechanism that cancels the inhibition of odontoblast proliferation by DEX in the Ift88 knocked-down KN3 cells.