Sonic hedgehog (Shh) signalling is one of the key pathways that promote ventral cell fate identity in the developing neural tube. Whereas some cells strictly require high levels of Shh activity for ventral specification, others can be specified by intermediate or low Shh activity levels over time. Now, Tamara Caspary and co-workers investigate the role of Inpp5e, a ciliary inositol polyphosphate-5-phosphatase that is thought to positively regulate Shh signalling, in allowing cells to sense the duration of Shh signalling. They find that a null mutant of Inpp5e (Inpp5erdg/rdg) shows an expansion of ventral cell fates by E10.5, suggesting that Inpp5e negatively regulates the Shh response. Yet ventral patterning in Inpp5erdg/rdg embryos recovers by E12.5, and this depends on the presence of Gli3, a repressor of Shh signalling. However, in mutants of the Shh activator smoothened, the Inpp5erdg/rdg mutation only rescues the expression of markers that are induced by intermediate levels of Shh, but not the expression of those that require high Shh concentrations. Therefore, Inpp5e is not simply a negative regulator of Shh. Additionally, Inpp5e loss promotes inhibitors of Shh signalling to associate with cilia, thus confirming its previously known roles in promoting the Shh response. Collectively, these results indicate that Inpp5e acts as both a positive and negative regulator of Shh function, and attenuates Shh signalling to prevent the untimely expression of ventral specification factors.