Lastly, the next 20 proteins showed random behavior identified in this targeted run, most commonly represented by proteins which are naturally most abundant in the human proteome like actin, tubulin, and trypsin hits. Figures and show that Jurkat cells treated for 30 mins are distinguishable from cells that are treated for 4 hours, and this separation is due to the different type of pathways that had been activated upon PMAi treatment. The separation of the cells by PCA is not as clear as in the case where we compared untreated and treated cells -most likely due to two facts: one is that this analysis is based only on 95 targeted proteins which are not very abundant, and the other most likely due to cells having a similar proteome level at both the 30 min and the 4-hour mark of PMAi treatment. Differentially expressed proteins from this data provide evidence that several pathways which are responsible for mitotic regulation, kinase activity, G1/S phase cell cycle/division, cellular response to oxygen containing compound and P53-signaling are more prominent after 4 hours of drug treatment and that these pathways show secondary response to drug activity. Output from STRING cluster analysis on the differentially expressed proteins are summarized in Tables and. The next experiment that we performed demonstrates SCREEN's ability to distinguish cancer cell types that can be treated by drug and those that are resistant to drugs. We used HL60 cancer cell line as an example of Doxorubicin treatable cancer and the MX2 cancer cell line that is multi drug resistant. This experiment was designed to show that SCREEN can distinguish essentially the same type of leukemia cancer cells that differ only by its drug resistance to doxorubicin . The cancer cells were sorted by the standard FACS 2x2 and 4x4 sorting patterns to prove that the sorting pattern doesn't impact SCEEEN's ability to separate these cell types. In Figures and respectively with the two types of FACS sorting patterns, SCREEN shows clear differences between the two states of the same leukemia cancer cells.