PTMScan experiments revealed the significantly increased phosphorylation levels at residues Thr308/309/305 in Akt1/2/3, Ser472 in Akt3, Ser2448 in mTOR, Ser246 in PRAS40; Thr37 and Thr46 in both 4E-BP1 and 4E-BP2, Thr23 in 4E-BP3; Ser235, Ser236, Ser240, Thr241 and Ser244 in S6, Ser376 in IKKγ, Ser21 in GSK3α, and Ser552 and Ser675 in β-Catenin (Table 3), which might stimulate and magnify PI3K/Akt signaling, and its downstream mTOR, NFκB, and canonical Wnt pathways to contribute to tumor progression. The gene discussed is NFKB1; the disease is neoplasm.