Interestingly, both inhibition of PI3K and AKT led to increasing nuclear FOXO1 and IGFBP1 levels in response to treatment with medroxyprogesterone acetate and dibutyryl cAMP, supporting evidence that the increased PI3K/AKT pathway is involved in the reduced decidual response in endometriosis [113]. This evidence concerns the gene AKT1 and endometriosis.