The mouse HoxA3 and HoxD3 genes are paralogs that occupy equivalent positions in their respective Hox gene clusters and share roughly 50% identity in their protein coding sequences. Mice with defects in HoxA3 have deficiencies in pharyngeal tissues, whereas mice with defects in HoxD3 have deficiencies in the axial skeleton, suggesting quite different functions for the paralogs. Thus, it came as a surprise when it was found that replacing a defective HoxD3 gene with the normal HoxA3 gene corrected the deficiency, as did the reciprocal experiment of replacing a mutant HoxA3 gene with a normal HoxD3 gene. Neither transplaced gene, however, could supply its normal function; that is, a normal HoxA3 gene at the HoxD3 locus could not correct the deficiency caused by a mutant HoxA3 gene at the HoxA3 locus. The same was true for the HoxD3 gene. If the HoxA3 and HoxD3 genes are equivalent, how do you suppose they can play such distinct roles in development? Why do you suppose they cannot perform their normal function in a new location?