The deletion of Igf2 in SSPCs (Prx1+ and Osx+), not osteoblasts (Ocn+) lead to the SRS-related bone deformities via downregulating Stat3 and can be rescued by the activation of STAT3, which offers a therapeutic approach for treating skeletal disorders in SRS patients by modulating the JAK-STAT pathway. Here, IGF2 is linked to Silver-Russell syndrome.