Thus, to clarify whether HIV-1 infection activates or inactivates pro-cancer pathways in cervical cells, we interrogated the global phosphorylation landscape of cells exposed to secretome of primary CD4+ T-cells infected with a replication-competent HIV-1 strain and uninfected controls similar to the workflow above for abundance proteomics (Figure 1B). The gene discussed is CD4; the disease is HIV-1 infection.