Additional mechanistic work in breast and lung cancer cell lines suggests the effect could also be caused by damaging mitochondria and deactivating the PI3K/Akt/mTOR (phosphatidylinositol 3-kinase/Ak strain transforming/mechanistic target of rapamycin) and MAPK/ERK (mitogen-activated protein kinase/extracellular signal-regulated kinases) pathways [137,138]. Here, MTOR is linked to lung carcinoma.