Britschgi et al. also found that EGFR inhibition only partially reduced TMEM16A overexpression-induced cell viability, and EGFR activation partially reversed the inhibitory effect of TMEM16A inhibitors on cell viability in breast cancer cells, suggesting that TMEM16A activates additional signaling pathways that are involved in cell viability [42]. This evidence concerns the gene EGFR and breast cancer.