AKT1 and non-small cell lung carcinoma: In alveolar type II cell-derived pulmonary adenocarcinomas (PACs), AKT-dependent nicotine-induced resistance to apoptosis was due to the upregulation of survivin (also known as BIRC5) and X-linked inhibitor of apoptosis (XIAP; also known as BIRC4) [105], whereas α7nAChR-mediated stimulation of NSCLC cell proliferation is through activation of β-arrestin–SRC (Figure 2) [106].