Oncogenes, also known as “cancer-promoting genes,” are specific genes whose mutations can lead to excessive proliferation of cells and lead to the development of cancer. These genes are divided into classes based on their “cancer-promoting” abilities (Alberts 2007). Proto-oncogenes represent the first class of genes. They cause a “gain-of-function mutation” that can lead a cell to a proliferative form of cancer (Alberts 2007). The resulting mutant, which is therefore “hyperactive or overexpressed” is the oncogenic form (Alberts 2007). The second class of these genes is one that causes a “loss-of-function mutation.” These are tumor suppressor genes, which can also lead to cancer. Both of these classes of genes have similarities in how they contribute to cancer proliferation and are therefore considered “sides of the same coin” (Alberts 2007). One of the recent developments in the research behind oncogenesis and its relation to cancer is the “oncogenic addiction” theory. This theory explains the phenomenon of “a tumor cell apparently showing dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “turn off the crucial addiction pathway,” which in theory should negatively affect or inhibit cancer, “while sparing normal cells that are not as addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and to see that there is tolerance without “obvious consequences” (Sharma & Settleman 2007). This is the concept of "dependency" in cancer, and the dependency on particular genes to activate proliferous... half of the article... needs to be developed to begin this study, we can deduce from past research the stages at which it might be the determination of these relationships was carried out. After developing a line in which an adequate assay can be performed, where Src phosphorylation can be analyzed, western blotting would be the first important step in this experiment (Pillay et al. 2009). Western blot would be used here to determine the levels of Src-kinase and phosphorylated Src-kinase in tumor cells (Pillay et al. 2009). Cell lysates would be immunoprecipitated and analyzed for these levels as well as EGFR levels in the cells (Pillay et al. 2009). After the samples are transferred to the correct membrane, a designed monoclonal antibody (mAb) would be used to probe phosphorylated Src-kinase. Similarly a mAb would be used to probe the attached EGFR (Pillay et al. 2009).