Becn2, also known as beclin 2, is a mammalian-specific member of the macroautophagy/autophagy family. It plays a crucial role in multiple biological processes, mainly through its involvement in non-canonical autophagy pathways. This gene is important in the regulation of innate immune signaling, metabolism, and endolysosomal degradation of certain receptors, which has implications for various diseases [2,4].

Loss-of-function experiments, especially in KO mouse models, have revealed significant insights into Becn2's functions. Mice lacking Becn2 showed enhanced activities of NLRP3, AIM2, NLRP1, and NLRC4 inflammasomes, promoting alum-induced peritonitis, which was rescued by CASP1 ablation, indicating its role as a negative regulator of inflammasome activation [1]. Becn2-deficient mice also developed splenomegaly, lymphadenopathy, elevated proinflammatory cytokine production, and spontaneous lymphoma development, due to the failure to degrade MAP3K7/TAK1 and MAP3K3/MEKK3 through a non-canonical autophagy pathway [2]. Additionally, Becn2 deletion protected mice from cocaine-stimulated locomotion and reward behaviors by increasing presynaptic dopamine receptor 2 autoreceptors in dopamine neurons [3].

In conclusion, Becn2 is essential for maintaining normal physiological functions through its role in non-canonical autophagy. The study of Becn2 KO mouse models has provided valuable information on its functions in inflammatory diseases, cancer, and drug-related behaviors, suggesting it could be a potential therapeutic target for these disease areas.