The primary cilium is an antenna-like structure present at the surface of most cells and necessary for normal development. In particular, it is required for Shh signalling, a crucial developmental pathway. However, the molecular mechanisms underlying the connection between the cilium and Shh transduction remain elusive. To address whether the ciliary localisation of Gli2, a transcriptional effector of the Shh pathway, is required for its activation, Aimin Liu and colleagues (p. 1651) generated a knock-in mouse strain in which Gli2ΔCLR, a non-ciliary variant of Gli2 that retains transcriptional activity and responds to its inhibitor Sufu in vitro, is expressed in a similar pattern to endogenous Gli2. Shh signalling is compromised in Gli2ΔCLR mutants and is not restored by the pharmacological activation of Smo, the co-receptor that transduces the Shh signal, in vitro or by the depletion of Ptc1, the Shh receptor that inhibits Smo, in vivo. Furthermore, the authors show that Gli2ΔCLR activates Shh targets at the same level as endogenous Gli2 in the absence of Sufu, indicating that the impaired Shh signalling observed in Gli2ΔCLR mutants results from an impaired ciliary-dependent release from Sufu inhibition. In summary, these findings reveal that the ciliary localisation of Gli2 is required for its activation, highlighting the importance of the primary cilium as a signalling compartment.