Silent mutations in the tumor suppressor gene TP53 and/or the retinoblastoma gene RB1 have been reported to be the main causes of the development of sporadic OS.71In vitro experiments comparing MSCs with malignant OS cells, as well as in vivo studies using transgenic mice with targeting p53 and Rb (retinoblastoma gene RB1; retinoblastoma protein) silencing in MSCs, have elegantly demonstrated that when p53 alone was deleted, the incidence of OS could reach 60%.72 Another function of p53 in suppressing tumor is to act as ‘a guardian of differentiation'.59 This evidence concerns the gene TP53 and neoplasm.