As well as demonstrating synergy between GDC-0032 and tamoxifen or fulvestrant treatment in tumors that were resistant to treatment with GDC-0032 alone, where the combined treatment lowered FOXM1, we have also demonstrated increased cell viability in drug-treated cells overexpressing FOXM1C and synergism between FOXM1 depletion and PI3Kα inhibition in tumor models with acquired or engineered resistance to PI3Kα inhibitors. Here, FOXM1 is linked to neoplasm.