BECN2 (beclin 2) is a mammalian-specific autophagy-related protein that regulates two distinct lysosomal degradation pathways with significant implications for cellular homeostasis and disease. The protein functions as both an autophagy regulator and a controller of G-protein coupled receptor (GPCR) turnover 1. BECN2 forms antiparallel homodimers through its coiled-coil domain but preferentially interacts with ATG14 to form more stable heterodimers, facilitating autophagosome formation through a mechanism distinct from its paralog BECN1 2. The protein mediates GPCR degradation by interacting with GPRASP1/GASP1, preventing receptor recycling and contributing to drug tolerance, particularly for cannabinoid receptors 3. BECN2 also serves as a negative regulator of innate immune signaling by targeting key kinases MEKK3 and TAK1 for degradation through an ATG9A-dependent pathway, with deficiency leading to increased inflammation and lymphoma development 4. Unlike BECN1, BECN2 does not significantly contribute to mitophagy 5. Additionally, BECN2 functions as a host antiviral factor by facilitating endolysosomal degradation of viral GPCRs, protecting against viral oncogenesis 6. These diverse functions highlight BECN2's critical role in maintaining cellular homeostasis and preventing pathological processes.