BCL2L10 is a multifunctional member of the BCL-2 protein family that exhibits context-dependent roles in cancer. In hepatocellular carcinoma, BCL2L10 functions as a tumor suppressor by suppressing cell growth, metastasis, and angiogenesis through inhibition of JAK-STAT3 signaling 1. Similarly, in gastric cancer, BCL2L10 promotes apoptosis through mitochondrial pathways and acts as a tumor suppressor 2. In ovarian cancer, BCL2L10 also demonstrates tumor suppressive properties by regulating Aurora kinase A stability and arresting cell cycle at G0/G1 phase 3. However, in melanoma, BCL2L10 exhibits pro-tumorigenic effects by increasing cell migration, invasion, and vasculogenic mimicry through ERK phosphorylation and upregulation of uPAR and matrix metalloproteinases 4. BCL2L10 is frequently hypermethylated in acute myeloid leukemia (45%) and therapy-related myeloid neoplasms, leading to silencing of this pro-apoptotic gene 5. Genetic variants, particularly the Leu21Arg polymorphism, are associated with reduced risk of developing therapy-related myeloid neoplasms and myelodysplastic syndromes 6. In hepatocellular carcinoma, BCL2L10 regulates autophagy by binding to Beclin 1 and modulating PI3K/AKT signaling 7. The protein also plays essential roles in oocyte maturation in buffalo models 8.