CYP11A1-overexpressing Caki-1 cells showed sustained activation of JNK and p38 along with inhibition of p-ERK and p-C-Raf, supporting our hypothesis that CYP11A1-induced oxidative stress may activate JNK-p38 pathways, specifically promoting apoptosis in the cancer cell line. This evidence concerns the gene CYP11A1 and cancer.