ASF1B and neoplasm: More importantly, MK2206 (an AKT-specific inhibitor), significantly inhibited the effects of ASF1B-overexpressing cell lines on tumor cell proliferation (Figure 6C) and migration (Figure 6D) in vitro, suggesting that AKT played a pivotal role in biological function of ASF1B in promoting lung cancer progression, and ASF1B promoted malignant behavior of LUAD cells by regulating the phosphorylation of AKT.