Thus, mechanistically, drug inhibition of HMGCR can decrease cholesterol synthesis, thereby attenuating cell proliferation, suppressing tumor progression, and inducing cell senescence by negatively regulating growth-promoting signals, including RAS, PI3K/AKT, RAF/MEK/ERK1/2, Hippo, and Wnt/β-catenin signaling cascades (81–83). This evidence concerns the gene AKT1 and neoplasm.