A possible mechanism might be that EGFR, an oncogene, played an important role in carcinogenesis and tumor progression via activation of the RAS/RAF/MEK/MAPK and the PI3K/AKT/mTOR pathways if mutated [45, 46] and that the incidence of EGFR mutation may be up-regulated by enhanced activation of certain pathways during the progression of tumors from a non-solid GGO to a part-solid pattern. The gene discussed is MTOR; the disease is neoplasm.