Mice with the fused toes (Ft) mutation - a 1.6 Mb chromosomal deletion encompassing six genes - exhibit phenotypes reminiscent of disrupted Hedgehog (Hh) signalling. Vierkotten et al. have individually knocked out these genes in mice to identify which one is involved in Hh signalling. On p. 2569, they reveal that the loss of fantom (Ftm) accounts for most defects in Ft mice. Importantly, they report that Ftm localises to the ciliary basal body where it functions as a novel component of cilia-related Hh signalling - regulating the Gli3 activator (Gli3A) to processed Gli3 repressor(Gli3R) ratio (Gli transcription factors act downstream of Hh). In Ftm mutant mice, Gli3 levels increase; however, it remains unprocessed, altering the ratio of Gli3A:Gli3R and consequently Hh transcriptional output. Interestingly, Ftm is not required for cilia assembly;however, cilia numbers are reduced where morphogenetic processes occur and thus cilia-coupled signalling might be required for cilia maintenance. In Drosophila, Hh signalling occurs independently of cilia;unsurprisingly, a fly Ftm homologue hasn't been identified.