These subtypes illustrate some underlying molecular signatures of the disease; ER and PR overexpression lead to cell cycle progression via the estrogen/ER pathway, while in HER2-positive breast tumors, HER2 gene amplification or protein overexpression activates the PI3k/AKT/mTOR and RAS/RAF/MAPK pathways, stimulating cell proliferation, differentiation, and survival [54,55,56]. The gene discussed is AKT1; the disease is breast neoplasm.