Based on the data showing that enforced expression of AMPK-β1 elevates AMPK activity but decreases AKT, ERK and JNK activities as well as abrogates its oncogenic capacities in cell growth, migration, invasion and sensitizing chemoresistant ovarian cancer cells to cisplatin-induced cell apoptosis, AMPK-β1 may be a potential therapeutic target in advanced ovarian cancer treatment. This evidence concerns the gene PRKAA2 and ovarian carcinoma.