“…Inhibition of EGFR mutants leads to increased cell death mediated by an apoptotic pathway that is dependent upon Bim, a Bcl-2 family member that is pro-apoptotic and regulated by Erk signaling (Costa et al, 2008;Cragg, Kuroda, Puthalakath, Huang, & Strasser, 2007;Deng et al, 2007;Gong et al, 2007). Although most patients tolerate erlotinib and gefitinib, some patients experience serious side effects such as diarrhea, rash, nausea and interstitial lung disease (Makris et al, 2007;Shah et al, 2005;Shepherd et al, 2005). Patients may have primary resistance due to EGFR drug-resistant mutations, such as EGFRvIII, which is a constitutively active form of EGFR caused by the deletion of exons 2 -7 (Greulich et al, 2005;Inukai et al, 2006;Maheswaran et al, 2008;Prudkin, Tang, & Wistuba, 2009;Wu et al, 2008), mutations in downstream signaling pathways that co-occur with EGFR mutations, such as the PI3K catalytic subunit, PIK3CA (Kawano et al, 2006), or mutations that occur in other downstream genes, such as k-Ras and b-Raf (Brose et al, 2002;Linardou www.intechopen.com et al, 2008;Mok et al, 2009;Pao et al, 2005b;Wheeler, Dunn, & Harari, 2010;.…”