Further studies reveal that GASP1 interacts with insulin-like growth factor 1 receptor (IGF1R) to prevent the MDM2-mediated ubiquitylation and degradation of IGF1R, promoting malignant phenotypes of breast cancer cells and decreasing their cellular response to paclitaxel by activating its downstream signaling pathways, such as NF-κB, PI3K/AKT, and MAPK/ERK pathways. This evidence concerns the gene NFKB1 and breast carcinoma.