The kinase activity of LKB1 is the only biological means to protect NSCLC cells against AICAR treatment, and we demonstrated that this activity is capable of promoting TIF-IA-mediated pre-rRNA synthesis following AICAR treatment in H157-LKB1-WT cells by actively recruiting TIF-IA into the nucleus. Here, RRN3 is linked to non-small cell lung carcinoma.