Primary cilia are sensory organelles understood to play important roles throughout development, as evidenced by the spectrum of neurodevelopmental phenotypes observed in instances of ciliary dysfunction (termed ciliopathies). Recent research indicates that in the adult brain, primary cilia may play roles in excitability, maintaining synaptic connectivity, and even form specialised synapses capable of altering the transcriptional landscape of neurons.To further understand the role of cilia in postmitotic neurons, we generated human induced pluripotent stem cell lines (hiPSCs) with NPHP1-/- and CEP290-/- mutations, and derived induced neurons (iNeurons) from these.In accordance with other cell types, the NPHP1-/- iNeurons show longer cilia whereas the CEP290-/- iNeurons lack a primary cilium. Despite contrary ciliary morphologies, surprisingly these lines showed very similar basal network activity when differentiated on microelectrode arrays: characterised by elevated network burst rates and shorter network bursts; with no overall change to the mean firing rate with respect to the control. This pattern bore similarities to how network rearrangement occurs during homeostatic plasticity induced through suppression of activity, prompting us to further investigate this connection.We determined that at both the functional and structural level, NPHP1-/- and CEP290-/- iNeurons do not respond significantly to induction of homeostatic plasticity. Although the precise mechanism underlying this is currently unknown, this data indicates an important role for functional primary cilia in homeostatic molecular remodelling. These results suggest that homeostatic plasticity could be altered in brain-related ciliopathies, and indicate a novel role for the primary cilium in the normal establishment of homeostatic plasticity.