However, the NPM-ALK-induced activation of mammalian target of rapamycin (mTOR), either transduced through the mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, or to a much less degree, through the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway has been shown to contribute to the tumorigenesis of ALCL [22,23]. This evidence concerns the gene MTOR and anaplastic large cell lymphoma.