Since hnRNP A1 and A2 are reportedly overexpressed in lung cancer [18, 19], and depletion of hnRNP A2 reduces AKT activity and Slug expression in NSCLC cell lines [20], we postulated that hnRNP A1 and A2 may regulate the alternative splicing of Tid1 to modulate tumorigenesis in human NSCLC. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.