Although Tat could activate PI3K/AKT-dependent survival pathways in KS cells [45], in this study, we showed that in Tat-transduced vIL-6-expressing cells, inhibition of PI3K/AKT and overexpression of PTEN or GSK-3β signal efficiently suppressed the enhanced effect of Tat on vIL-6-induced angiogenesis and tumor development in vivo. Here, AKT1 is linked to neoplasm.