Since it has been already described that HIF-1α, GLUT1 and CAIX are required for CSC survival and tumor aggressiveness, and that we have recently shown that P-cadherin is also involved in the maintenance of stem-like properties of basal-like breast CSCs, we decided to evaluate the effect of the inhibition of all these molecules, alone or in combination, on the mammosphere forming efficiency (MFE%) of the SUM149 breast cancer cell model (Figure 6). The gene discussed is SLC2A1; the disease is neoplasm.