We also provide evidence that FOXM1, presumably by virtue of its interaction with the retinoblastoma (Rb) cell cycle progression and tumor suppressor protein, promotes β-galactosidase (β-gal+) activity in myeloma – the classic Rb-regulated phenotype of cellular senescence that is mechanistically linked to relapsed cancer by means of acquired drug resistance, cancer dormancy and cancer stemness [14]. Here, FOXM1 is linked to cancer.