It has also been shown that cyclin D1 expression which mediates proliferation of tumor cells is a result of EGFR autophosphorylation leading to its complexing with PI3K and subsequent activation of ERK and AKT, and that under stress conditions such as growth factor deprivation, tumor cell dormancy is promoted as a result of decreased active AKT and cyclin D1 levels due to failed ERK-PI3K complex formation [59]. This evidence concerns the gene AKT1 and neoplasm.