The tabby syndrome in the mouse (which is common to the sex-linked gene for tabby and autosomal genes for crinkled and downless) affects the coat, the sinus hairs, the teeth, many glands and some surface features like tail rings, plicae digitales and the papilla vallata of the tongue. All these structures develop by the downgrowth of solid epithelial buds into the underlying mesenchyme. Organs which arise by invagination (like the neural tube or the otic vesicles and certain glands) are not affected by the tabby syndrome. The rudiments of glands and sinus hairs are reduced in size, and if reduction goes beyond a critical point, stunted organs are formed or, more commonly, the rudiments regress altogether. The same is true for the teeth and apparently for the whole syndrome. Measurements show the same situation inTa♂♂(andTa/Ta♀♀) and in heterozygousTa/ + ♀♀. As inTa♂♂ andTa/Ta♀♀ there cannot be any doubt that a threshold mechanism is involved, there is no reason to assume that, inTa/ + ♀♀, the identical defects are derived clonally from ancestral cells in which the Xchromosome carrying the normal allele has been inactivated. Whereas theTa/ + phenotype does not give any evidence that theTalocus is involved in X-chromosome inactivation, the possibility cannot be ruled out that, if inactivation should actually take place on the cellular level, the macroscopic phenotype could be the result of intercellular interactions along with the effects of threshold mechanisms.