Lung adenocarcinoma comprises about 80% of all lung cancer cases. Metastasis is the major reason for death among lung adenocarcinoma patients. Thus, understanding the determinants of metastasis is critical to improve patient outcomes. Bcl-2–like protein 13 (BCL2L13) is known as a mitophagy mediator that is linked to ceramides lipid metabolism via the inhibition of ceramide synthase 2 and 6 activity. BCL2L13 can also regulate apoptosis. Our preliminary clinical data suggested that not only the BCL2L13 gene expression was significantly downregulated in lung cancer patients with poor survival, but also the BCL2L13 protein expression was significantly reduced in metastatic sites compared to the primary lung tumor in lung cancer patients. We hypothesized that BCL2L13 regulates NSCLC metastasis through mechanisms deponent on mitophagy and detachment-dependent cell death (anoikis). Here, for the first time, we provide evidence that BCL2L13 is involved in regulation of lung adenocarcinoma metastasis via mitophagy-dependent regulation of epithelial to mesenchymal transition (EMT) and anoikis resistance in context of CerS2 and CerS6 activity. Our investigations showed that BCL2L13 is required for the induction of mitophagy in human and mouse lung adenocarcinoma cells. Furthermore, we showed that BCL2L13 knockdown potentiates the TGFβ1- induced EMT and subsequent metastasis and induces anoikis resistance in these two lung adenocarcinoma models. Also, the oxygen consumption rate and hallmarks of mitochondrial bioenergetics (baseline respiration, maximal respiration, spare capacity, non-mitochondrial respiration, and ATP production) were reduced in BCL2L13 knockdown cells, indicating presence of the Warburg effect. Lipidomics findings showed that BCL2L13 knockdown increases levels of CerS2 and 6 related ceramides (C16, C22, and C24) under attached conditions while BCL2L13 overexpression increases levels of these ceramides under anoikis conditions. Lack of BCL2L13 increased while BCL2L13 overexpression decreased the expression of FAK, p-FAK (Tyr 576/577), and p-FAK (Tyr 925) in lung adenocarcinoma cells under anoikis conditions. Also, we showed that NIX and BNIP3 localization was increased while BAX and truncated BID localization was decreased in mitochondria in BCL2L13-KD cells under anoikis conditions. Taking our findings together, we identify BCL2L13 as an important contributor to lung adenocarcinoma metastasis through mitophagy-dependent regulation of EMT and intrinsic apoptosis-dependent anoikis resistance in context of CerS2 and CerS6 activity. Correspondingly, these effects are exerted by BCL2L13 through its role in regulation of ceramides synthesis. Targeting or mimicking BCL2L13 could be considered as a promising novel approach to enhance responses of therapy via sensitizing lung adenocarcinoma cells to undergo anoikis. This could significantly help reduce the metastasis rates in patients with lung adenocarcinoma.