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. The gene discussed is AKT1; the disease is neoplasm.