MTOR and lung carcinoma: This hypothesis is supported by previous studies reporting that decreased FASN activity by C75 and (−)-epigallocatechin-3-gallate (EGCG) can induce apoptosis through the downregulation of phosphorylated and total protein levels of the epidermal growth factor receptor (EGFR) and its downstream phosphorylated form of cellular signaling pathways, including extra cellular-signal-regulated kinase (p-ERK1/2), p-AKT, and p-mTOR in A549 lung carcinoma cells [34].