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. The gene discussed is AKT1; the disease is breast cancer.