We verified the various rewiring events using the existing literature and confirmed the validity for the above mentioned network changes. p53 is a tumour suppressor and controls the regulation of PUMA. PUMA induces apoptotic signals inside the cells. Less activity of PUMA leads to apoptosis deficiency which in turn leads to the increased risk of cancer [31]. We also realised that SMAC down-regulates XIAP and XIAP down-regulates Casp3, a pro-apoptotic protein. So if SMAC is working properly, there will be more cell death leading to less tumorigenic behaviour by cells. But if SMAC is not able to down-regulates XIAP, there will be less apoptosis and so more chances of cancer [2]. We also came across literature evidence highlighting the critical role of Casp8 for affecting breast cancer directly [5,32]. STAT3 interacts with various molecules involved in programmed cell death, regulating their functions including MOMP formation, which leads to the release of the cytochrome c [33]. XIAP inhibits the processing of Casp8. In fact, proteolytic processing of several caspases, including Casp9, is not allowed in the presences of XIAP. The lack of processing of Casp8 and Casp9 allows them to interact with Casp3 and promote apoptosis [34]. TNFR activates the Stat3 signalling. The stimulation of TNFR leads the phosphorylation of the Stat3 and Stat5b and the phosphorylated molecules are trans-located into the nucleus [35].