In addition to ER stress induction, high concentrations of EGCG can also decrease cell viability via a variety of mechanisms across different cancer cells, such as inhibiting fatty acid synthase (FASN) activity and epidermal growth factor receptor (EGFR) signaling to induce apoptosis in human adenocarcinoma lung cancer cells [48], inducing cell cycle arrest and impeding EGFR signaling to evoke cell cycle arrest and apoptosis in human epidermoid carcinoma cells [49], and inactivating β-catenin signaling to increase cell death of human skin cancer cells [50]. This evidence concerns the gene EGFR and squamous cell carcinoma.