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Newer therapies for BCL have improved the prognosis for many patients. However, approximately 30% with aggressive BCL either remain refractory or ultimately relapse. These patients urgently need other options. This study shows how calcium\/calmodulin\u2010dependent protein kinase II delta (CAMKII\u03b4) is pivotal for BCL development. In BCL cells, ablation of CAMKII\u03b4 inhibits both lipolysis from lipid droplets and oxidative phosphorylation (OXPHOS). With lipolysis blocked, BCL progression is markedly suppressed in two distinct BCL mouse models: MYC\u2010driven <jats:italic>E\u00b5Myc<\/jats:italic> mice and <jats:italic>Myc\/Bcl2<\/jats:italic> double\u2010expressed mice. When CAMKII\u03b4 is present, it destabilizes transcription factor Forkhead Box O3A (FOXO3A) by phosphorylating it at Ser7 and Ser12. This then permits transcription of downstream gene IRF4 \u2013 a master transcription factor of lipid metabolism. The CAMKII\u03b4\/FOXO3A axis bolsters lipid metabolism, mitochondrial respiration, and tumor fitness in BCL under metabolic stress. This study also evaluates Tetrandrine (TET), a small molecule compound, as a potent CAMKII\u03b4 inhibitor. TET attenuates metabolic fitness and elicits therapeutic responses both in vitro and in vivo. Collectively, this study highlights how CAMKII\u03b4 is critical in BCL progression. 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