An interesting discussion point is added by experimental evidence for the possible direct connection between ATM and LMNB1 happening in the nuclear compartment whilst the highly ordered processes of chromosome segregation and cell division is ongoing. Chromosome alignment,movement and segregation during Bicalutamide Androgen Receptor inhibitor cell division include relationships between the mitotic spindle and the kinetochore through microtubule depolymerization/assembly. Significantly, we unveiled differential expression of tubulins and Heat Shock Proteins in both proteomics dataset. Even though the expression of some cytoskeleton proteins and HSPs could be related to their abundance and for that reason with their easier accessible identification by mass spectrometry experiments, in our opinion the particular presence of centrosome components, like tubulins, and Hsp 70 and 90 in our cellmodels is associated with their function in cell cycle control, cell death and aggresome selling formation as defined in many literature papers and already noticed in our previous work. Mediators of stress reaction indeed manage centrosome inactivation checkpoint and use stress inducted centrosome fragmentation or sound for removing damaged cells. The role of HSPs in cell cycle get a grip on and in signal Retroperitoneal lymph node dissection transduction networks has been indeed described and given both to Hsp 90 and Hsp 70. Particularly Hsp 70, as binding companions of hSNM1B/ Apollo, a protein with stimulating impact on ATM substrate phosphorylation in a reaction to DNA damage, results indirectly implicated in the maintenance of genome stability. Recent angiogenic inhibitor studies have also revealed the involvement of Hsp 70 in the maintenance of cytoarchitecture. Zhang X. and colleagues have indeed described the unexpected role of Hsp 70 to promote aggresome development through the interaction with the cochaperone ubiquitin ligase Carboxyl terminal of Hsp70/Hsp90 interacting protein. In summary they were qualified by the participation of tubulins and HSPs in cell surveillance mechanisms as additional implementing checkpoints recruited and activated by stress stimuli, thus explaining in part their differentially expressed levels in ATM lack in our proteomic observations. Among the proteins whose levels were influenced by ATM expression andMG132 treatment andwere analyzed by western blot, Matrin 3 was already identified as crossreacting protein to phospho certain antibodies against known ATM/ATR substrates. Furthermore, Matrin 3 has been already described in literature as involved in early stage ofDSB reaction. In fact, treatment with the radiomimetic adviser neocarzinostatin andMATR3 depletion led to abnormal accumulation of cells at the S phase of the cell cycle. An upregulated protein expression was observed by us in L6ATMtreated cells by nLC MSE method.