In the present study, the IGF1 and IGFBP3 levels in the patient were far below normal levels, consistent with a model in which the duplication of GRB10 directly inhibits the phosphorylation of the IGF1R substrate and reduces the level of Grb10 expression to below normal limits, which may result in nervous system impairments such as growth delays and intellectual disabilities (ID) [23]. The gene discussed is IGF1R; the disease is Intellectual disability.