Future research is needed to explore the upstream and downstream molecular pathways associated with KRAS gene mutations in adenomyosis, such as phosphatidylinositol 3-kinase/phosphoinositide dependent kinase 1/Protein Kinase B (PI3K/PDK1/AKT) and Rapidly Accelerated Fibrosarcoma/Mitogen-Activated Protein Kinase/extracellular signal-regulated kinase (RAF/MEK/ERK) pathways [24,25], and find precision therapy targeting KRAS mutations. This evidence concerns the gene AKT1 and adenomyosis.