We observed the addition of FO and Se to Avastin treatment was crucial to induce: (1) decreases in the phosphorylation of multiple potent proangiogenic (growth) factors and their membrane receptors; (2) regulation of cytoplasmic PI3K-PTEN-AKT-TSC1/2-mTOR-70S6K-4EBP1, Ras-Raf-MEK-ERK, c-Src-JAK2-STAT3-TMEPAI-Smad, LKB1-AMPK, and GSK3β-β-catenin signaling; (3) inhibition of nuclear cyclin and cyclin-dependent kinases; (4) upregulation of tumor apoptosis, as well as; (5) inhibition of the HSP90, HIF-1α/HIF-2α, COX-2, SOD-1, and MMP-9, and; (6) suppression of the EMT and stemness in tumor. The gene discussed is STK11; the disease is neoplasm.