Considering that MDM2 has been demonstrated to mediate IGF1R ubiquitination degradation [26, 27], we thus suppose that GASP1 may destroy the interaction between IGF1R and MDM2, as demonstrated that our data showing that GASP1 knockout caused an enhanced interaction between IGF1R and MDM2 in breast cancer cells, thereby protecting IGF1R from MDM2-mediated degradation and post-transcriptionally up-regulating its expression. This evidence concerns the gene IGF1R and breast carcinoma.