Bone morphogenetic proteins (BMPs) regulate cell-fate decisions during embryonic development. But after birth, dysfunctional BMP expression is linked to some human diseases, like carcinomas. In lung cancer, BMPs are reactivated and suppress AMPK signaling. Mitochondrial stress activates AMPK to a ‘normal’ level, where it promotes cancer cell survival, but AMPK can induce cell death if ‘hyperactivated.' BMPs inhibit LKB1, a kinase that can hyperactivate AMPK, making BMPs a potential therapeutic target. So, researchers tested two BMP inhibitors as a combination treatment with mitochondrial targeting agents. In lung cancer cell lines that express LKB1, the combination treatment activated AMPK and suppressed cell growth. The combination treatment was increasing nuclear localization of the aptly named apoptosis inducing factor (AIF) in these cells, an effect that depended on LKB1 expression. Similarly, suppressing expression of a BMP protein in tandem with either of the mitochondrial targeting agents also increased nuclear localization of AIF. Lastly, the combination therapy was also able to enhance AIF nuclear localization and cancer cell death in cultured cells from patient tumors. While more work is needed, these results demonstrate the potential utility of this BMP inhibition combination treatment to treat lung cancer.