PKB/Akt is known to counteract suicidal cell death in part by phosphorylation of Bad, which fosters binding of Bad to 14-3-3 thus preventing insertion into the mitochondrial membrane. Along those lines, gain of function mutations of PKB/Akt have been detected in several tumors. PKB/Akt is regulated by the phosphoinositide dependent kinase PDK1 which may thus play an important role in regulation of cell survival and tumor growth. The present study has been performed to explore the role of PDK1 in tumor growth. As mice completely lacking functional PDK1 are not viable, hypomorphic mice expressing 10–25% of PDK1 (pdk1^hm) were compared to their wild type littermates (pdk1^wt). pdk1^hm and pdk1^wt were subjected to chemical cancerogenesis (intraperitoneal injection of 20 mg/kg 1,2-dimethylhydrazine followed by three cycles of 30 g/L synthetic dextran sulfate sodium for 7 days). Bad phosphorylation was determined by Western blotting. Following chemical cancerogenesis, pdkhm mice developed significantly less colonic tumors than pdkwt mice. According to Western blotting and immunohistochemistry, PDK1 deficiency decreased Bad phosphorylation. In conclusion, PDK1 deficiency decreases Bad phosphorylation and protects against the development of colonic tumors.