AKT1 and cancer: BTG2-mediated activation of NFκB via PI3K-Akt pathway was independent of p53 status in normal and cancer cells (Figures 4 and 5, and Additional file 2: Figure S2) such as HeLa (p53 low expresser due to HPV E6 & E7 gene expression), A549, wt-MEF and MCF7 cells (wt-p53), therefore, BTG2-regulated crosstalk between PI3K-Akt1 and NFκB pathways was active in a p53-independent manner.