Figure 3

Arsenic-mediated activation of EGFR signaling pathway. EGFR and several components of this pathway can be activated by arsenic exposure in human lung cells. This activation can be inhibited by EGFR-TKI, revealing a potential role for TKIs in the management of arsenic associated lung tumors, regardless of the mutational status of EGFR. As^III can also induce STAT3 inhibition by targeting JAK, while it can activate STAT3 trough JNK, contributing to AKT activation.