Given that FOXM1 is involved in endocrine resistance, expansion of stem-like cancer cells, stem cell self-renewal, cancer initiation and metastasis [5,6] it is conceivable that a switch from ERα-dependent to ERα-independent/HER2-dependent expression of FOXM1 enables disseminated ER+/HER2− to re-initiate tumor cell growth and metastasis formation in the presence of endocrine treatment, as is observed in patients with late recurrence and metastatic ER+/HER2− breast cancer. This evidence concerns the gene FOXM1 and breast cancer.