In addition, skeletal anomalies arising from Mir17-92 deficiency can be effectively ameliorated through genetic or pharmacological inhibition of TGF-β signaling, indicating a crucial role for elevated TGF-β signaling in the skeletal abnormalities of Feingold syndrome type 2, but the skeletal phenotype associated with Mycn-deficiency experiences only partial mitigation through Pten heterozygosity and fails to respond to TGF-β inhibition (97). This evidence concerns the gene TGFB1 and Feingold syndrome type 2.