These genetic mutations in NSCLC and SCLC are considered to be the major oncogenic drivers due to their ability to affect various upstream and downstream signaling molecules of numerous pathways, including the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway (PI3K/Akt/mTOR pathway); rat sarcoma virus gene (RAS)/rapidly accelerated fibrosarcoma (RAF)/MAPK or ERK kinase (MEK)/ERK pathway (RAF/MEK/ERK pathway); and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) transduction pathway (JAK/STAT pathway) [35]. This evidence concerns the gene MTOR and fibrosarcoma.