Altogether, the molecular mechanism underlying UA’s anticancer activity depends on EGFR signaling, which then signals to JAK2/STAT3, causing STAT3 to translocate to the nucleus to bind with the VEGF, MMP2, and PD-L1 promoters in order to block their transcription, thus inhibiting tumor angiogenesis, invasion, metastasis, and tumorsphere formation (Figure 7). The gene discussed is JAK2; the disease is neoplasm.