GROWTH is one of the fundamental aspects in the development of an organism. Classical genetic studies have isolated four viable, spontaneous mouse mutants¹ disrupted in growth, leading to dwarfism. Pygmy is unique among these mutants because its phenotype cannot be explained by aberrations in the growth hormone–insulin-like growth factor endocrine pathway^2–5. Here we show that the pygmy phenotype arises from the inactivation of Hmgi-c (ref. 6), a member of the Hmgi family⁷ which function as architectural factors in the nuclear scaffold⁸ and are critical in the assembly of stereospecific transcriptional complexes⁹. Hmgi-c and another Hmgi family member, Hmgi(y) (ref. 10), were found to be expressed predominantly during embryogenesis. The HMGI proteins are known to be regulated by cell cycle-dependent phos-phorylation which alters their DNA binding affinity¹¹. These results demonstrate the important role of HMGI proteins in mammalian growth and development.