In contrast, the Oncotag treatment resulted in sustained downregulation of the pro-oncogenic molecules such as PDGFRβ, eNOS, PLC-γ1, JNK, p38α, Fgr, transcription factors STAT2, STAT5, and anti-apoptosis factor HSP27 (Figure 5B) and, probably, in long-term decrease in tumor aggressiveness. The gene discussed is STAT5A; the disease is neoplasm.