MSCs/CCR7 made donor T lymphocyte in SLOs more ‘naive like’. The increased na ve phenotype may give explanation to the increased donor T cells in SLOs and less lymphocytes infiltration in the peripheral target organs. Therefore, it was justifiable that MSCs/ CCR7 made the T cells maintain in SLOs, and decrease infiltration in GvHD target organs. These results mean MSCs/CCR7 infusion spoiling the fourth supplemental Billingham’s tenets to inhibit GvHD development. Consistent with the recent studies, the immunomodulatory effect of MSCs/ CCR7 was not innate, and it could be induced by inflammatory stimulation. This may confer the inducible modulatory activity of MSCs/CCR7 in vivo. In the other words, acting as potent inflammation holder, MSCs/CCR7 might calm down the high immune process quickly and keep quiet in the normal physiological circumstance as well. These results showed that an appropriate INMAP level is physiologically necessary, abnormal level affecting the fate of cells. p21 is a key factor regulated by p53 in response to DNA damage, accumulating in cell nucleus owing to increasing gene expression after DNA damage. It binds to CDKs and suppresses their activity, leading to cell-cycle arrest at the G1/S or G2/M phase. Cell-cycle arrest induces the function of p21 in promoting error-free replication-coupled DNA double-strandbreak repair, as well as inhibiting DNA replication by binding with the proliferating cell nuclear antigen, DNA polymerase-d and several other proteins involved in DNA synthesis. In addition, p21 can promote apoptosis through both p53-dependent and p53- independent mechanisms under certain cellular stresses, inducing upregulation of the proapoptotic protein BAX and activation of tumour necrosis factor family members of death receptors. In a recent study, we detected the effect of INMAP overexpression in HEK293T cells, revealing that high level of INMAP represses p53 and AP-1 transcriptional activity in a dose-dependent manner. Therefore, biological activity of INMAP may be related to carcinogenesis through p53 and AP-1 pathways. It is clear that INMAP interacts with proteins such as NuMA, a protein required for the selective induction of p53 target genes and playing a crucial role in WZ8040 regulating p53 mediated transcription in response to DNA damage. Following DNA damage, the level of the NuMAp53 interaction gradually increases in a time-dependent manner. Binding to CDK8, NuMA also activates the downstream gene p21 and causes cell-cycle arrest. The ablation of NuMA attenuates the pro-arrested p21 gene induction following DNA damage, and consequently, cellcycle arrest is impaired. Notably, the clear determination on whether and how the functions of INMAP are involved with p53 signalling pathway is ponderable. The goals of this study were to assess whether a high level of INMAP may affect tumour growth and to explore the functional pathway of INMAP. We constructed a HeLa cell experimental model with stable overexpression of INMAP and analysed the frequency of micronuclei and degree of chromosome distortion induced by INMAP abnormal expression.