To define a mechanism through which the presence of caffeine caused an increase of cisplatin-induced apoptosis in the lung cancer cells, we determined the phosphorylation levels of CHK1 (Ser317/Ser345), ATM (Ser1981), and p53 (Ser15), three proteins involved in the DNA damage-induced signaling process (5,8), from both untreated and caffeine/cisplatin-treated HTB182 and CRL5985 lung cancer cells (Figure 4). The gene discussed is ATM; the disease is lung carcinoma.