We did not explore if BRM, the other ATPase subunit of SWI/SNF complexes could replace BRG1 in those complexes since these two enzymatic subunits are exclusive. It would be interesting if the BAF47 switch in the SWI/SNF and N-CoR-1 complexes could be correlated with involvement of BRM in the same complexes. From a personal communication from S. Albini it appears that BRM could play some specific roles during muscle terminal differentiation. Interestingly, N-CoR-1 has been implicated in muscle mass control and myogenesis. Since BAF47 can participate to different type of complexes, either involved in chromatin remodeling like SWI/SNF or in transcription repression like N-CoR-1, it is likely that this subunit plays a dual and complex roles in the transcriptional control. We were also interested in the role of individual SWI/SNF subunits in the irreversible cell cycle exit, since BRG1 and BAF47 are bona fide tumor suppressor genes. We have shown that these two subunits are present on cyclin D1 promoter in proliferation and upon U0126 differentiation induction. Interestingly, BrdU incorporation experiments indicate that cell cycle exit upon serum deprivation is not total for BRG1 or BAF47-depleted myoblasts, while BAF53a-depleted cells behave as control cells. For BRG1, similar results were reported by de la Serna et al.. Surprisingly, upon GM addition, only BAF47- but not BRG1depleted cells were able to re-enter cell cycle. At a molecular level, cyclin D1 is re-expressed in BAF47-depleted cells. Re-expression of cyclin D1 in the absence of BAF47 is in agreement with a previous study that showed that BAF47 is targeted to cyclin D1 promoter along with HDAC1 to repress its expression. The BAF47 effect on Cyclin D1 repression and cell cycle exit is specific and somehow not directly correlated to BAF47 requirement in myoblast differentiation since BRG1 and BAF53 do not modify permanent cell cycle exit but are, anyhow, essential in myoblast terminal differentiation. The different and complex roles played by SWI/SNF BAFs are far from being totally elucidated. The essential roles of BRG1 and BAF60c in myogenic differentiation have been already clearly demonstrated. Our present study demonstrates that BAF47 and BAF53a are also required for proper myogenic differentiation. We have shown that BAF47 could play a dual role both in permanent cell cycle exit and muscle gene transcription and it participates in different complexes involved in transcription regulation. BAF47 participation to these complexes varies upon differentiation that could represent a fine mechanism to tune transcription. We have also highlighted a specific role for BAF47 compared to BRG1 in the control of the irreversible cell cycle withdrawal, even if both of them are known as tumor suppressor genes. The specificity of BAF47 in cell proliferation control is probably the reason why this tumor suppressor is inactivated in almost all the rhabdomyosarcomas, while the BRG1 inactivation is less frequent. Cisplatin is an effective chemotherapeutic agent that is widely used against several types of solid tumors. However, its clinical use is limited by its potent nephrotoxicity.