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IGF-I, essential for normal human growth in utero and postnatally, mediates its effects through the IGF-I receptor (IGF1R). More than nine heterozygous mutations, including one compound heterozygous mutation, of the IGF1R gene have been reported in patients with varying degrees of intrauterine and postnatal growth retardation.

Severe Short Stature Caused by Novel Compound Heterozygous Mutations of the Insulin-Like Growth Factor 1 Receptor (IGF1R)