As our previous studies in triple-negative breast cancer cells indicated that loss of GPS2 was associated with a more aggressive phenotype due to hyperactivation of PI3K/AKT signaling (43), these results suggest that the concurrent upregulation of PI3K and MYC signaling, due to unrestricted ubiquitination of cytosolic and nuclear targets, may be contributing to the observed phenotype of GPS2-null cells. The gene discussed is GPS2; the disease is triple-negative breast carcinoma.