The formation of long-lived immune memory cells specific for pathogens is critical for the establishment of long-term immune protection against sweat cover future infections.BNIP3L/NIX and BNIP3, two functionally redundant BCL2 family members required for mitophagy, undergo significant upregulation after memory B cells are formed.Deletion of Bnip3l and Bnip3 leads to mitochondrial accumulation, and increases in oxidative phosphorylation and fatty acid synthesis, resulting in the loss of memory B cells.These observations suggest that after the formation of memory B cells, mitophagy is critical for clearing superfluous mitochondria to re-shape the metabolic programs, thereby protecting the metabolic Holders quiescence and longevity of memory B cells.