However, neuronal loss was not proposed to be the cause of the obesity phenotype in these mice. These studies using congenital mouse ciliopathy models indicate the importance of conditional approaches to address roles for cilia in specific CNS regions. One study looking at neuronal cilia function using conditional alleles in the CNS comes from work by Amador-Arjona et al.. In this work the authors analyze cilia in the CNS after development using a conditional allele of Intraflagellar transport protein 20. However, one concern from this study is that the Cre line used would result in cilia loss in all GFAP expressing cells and descendants, including astrocytes, oligodendrocytes and neurons and thus specific claims about neuronal cilia are limited. In agreement with the work presented here using an Emx1-Cre to ablate cilia on neurons these authors also observed a novel Riboflavin object recognition phenotype. In our cre reporter analysis and cilia immunofluorescence indicate prominent and specific Cre expression in both the cortex and hippocampus. It is interesting to note that in the Emx1-Cre Ift88D/D mutants the dentate gyrus has noticeably less cilia than its control counterpart, yet some cilia are still present. It is possible that these remaining cilia are simply derived from cells that do not express Emx1 or that there is a degree of incomplete expression of the Cre in these regions of the brain. In fact there are certain populations of neurons such as the cortical GABAergic lineage which have been shown not to express Emx1. Another possible reason for these remaining cilia in the dentate is that the adult neurogenic niche in the sub-granular zone remains intact in this Emx1-Cre conditional approach, which may populate the hippocampus with ciliated neurons. It is enticing to hypothesize that these cilia in the Riociguat (BAY 63-2521) mutant dentate gyrus are allowing mice to perform normally in a spatial memory paradigm such as the MWM. Perhaps the near complete loss of cilia in other regions of the hippocampus is enough to show deficits in both the aversive and recognition memory tasks of fear conditioning and novel object recognition.