Our results in vitro are consistent with work suggesting that the occurrence of hydrocephalus observed in response to Fgf2 treatment in vivo is not caused by a direct effect of Fgf2 on CPe secretion, but could be due, at least in part, to a decrease in CSF absorption caused by impaired function of the arachnoid villi, the main structure involved in this process [23]. Here, CPE is linked to Hydrocephalus.