It has been demonstrated that coordinated ectopic expression of OCT4, SOX2, KLF and c-MYC (OSKM) induces reprogramming of somatic cells pluripotency [44] while activation of individual core stem factors can contribute to tumorigenesis because the same pluripotency transcription factors are also integrated into different and separate networks that are associated with the formation of different cancer phenotypes [45–47]. The gene discussed is MYC; the disease is cancer.