Moreover, continued activation of PI3K/Akt signalling, which triggers mTOR, seems to contribute to the development and maintenance of an EGFR-resistant phenotype (Chakravarti et al, 2002; Vivanco and Sawyers, 2002; Bianco et al, 2003; Janmaat et al, 2003), and it has been found in tumour samples from cancers patients failed in EGFR-targeted therapy (Rojo et al, 2006). Here, AKT1 is linked to neoplasm.