For example, Saudi-type familial SD has been linked to the hammer-toe locus in mice [10], while Cenani–Lenz SD is associated with APC variations [59], missense alterations in FIBULIN1 are associated with brain atrophy-syndactyly syndrome [60], and genomic replications of the SHH enhancer ZRS lead to triphalangeal thumb polysyndactyly syndrome [61], Greig syndrome, acrocephalosyndactyly syndromes and other SD phenotypes linked with the GLI3 variants [62]. Here, GLI3 is linked to Salla disease.