Recent studies have identified several mechanisms by which cancer cells adapt to PI3K-targeted therapy, such as reprogramming of mitochondrial trafficking33 and upregulation of prosurvival proteins.17 Although it remains challenging to directly target protein–protein interactions between GAB2 and effectors, our results suggest that co-targeting IKKβ and PI3K pathways downstream of GAB2 might be a promising therapeutic strategy for ovarian cancer that overexpresses GAB2. This evidence concerns the gene PIK3CA and ovarian cancer.