In breast cancer, Rac1 has been reported to be overexpressed and hyperactive.18 Upon activation by guanine nucleotide exchange factors (GEFs), active (GTP-bound) Rac1 has been shown to increase cancer cell migration, proliferation, transcription and survival by activating a multitude of downstream effectors.19 To determine whether HACE1 controlled Rac activation in breast cancer cells, HACE1 was overexpressed in MCF7 breast cancer cell line (Figure 3c). The gene discussed is AKT1; the disease is breast cancer.