As we have determined that JNK is required for the evasion of Gli2 from proeasomal-ubiquitin degradation in response to PGE2 by phosphorylating Gli2 at Thr1546, we then set out to test whether JNK is involved in the Hh activation and the consequent proliferation of colorectal cancer cells elicited by PGE2. The gene discussed is GLI2; the disease is colorectal cancer.