Atg2b, or autophagy-related protein 2 homolog B, is a key factor in the autophagy pathway. Autophagy is an essential cellular process for degrading and recycling cellular components, which is crucial for maintaining cellular homeostasis, development, and response to stress [1,4,5,6,7].

In gene-knockout studies, mice lacking both Atg2b and Gskip, but not either alone, showed decreased hematopoiesis, resulting in in-utero death with anemia. The number of hematopoietic stem cells, especially long-term HSCs, in double-knockout fetal livers was significantly decreased due to increased cell death, although the remaining HSCs could still differentiate, but with low efficiency [2]. In ovarian cancer, inhibition of ACSS2 leads to the activation of SIRT1, which mediates the deacetylation of Atg2b, promoting autophagy and reducing malignancy and chemoresistance [1]. In gastric cancer, circDHX8 stabilizes Atg2B by preventing its ubiquitin-mediated degradation, facilitating cell proliferation and invasion [4]. In septic liver injury, ATG2B upregulated in LPS-stimulated BMSCs-derived exosomes attenuates injury by inhibiting macrophage STING signaling [3]. In sheep granulosa cells, Atg2B is associated with cell autophagy, and its overexpression promotes autophagy, while inhibition has the opposite effect [5].

In conclusion, Atg2b is vital for autophagy-related biological functions. Gene-knockout mouse models have revealed its role in hematopoiesis and its implications in various diseases such as ovarian cancer, gastric cancer, septic liver injury, and in the context of different genotypes in sheep granulosa cells. Understanding Atg2b provides insights into disease mechanisms and potential therapeutic targets for these conditions.