TCF3 and Burkitt lymphoma: mTOR signaling is essential for B cell development, GC reactions, and antibody responses.65–72 mTORC1 activity in GC B cells is dynamically regulated and has to be tightly controlled, as both hyperactivation and insufficiency impair GC function with reduced levels of BCL6 and AID expression.65,69,71,72 Supporting mTORC1’s central role, a recent CRISPR screen in Burkitt’s lymphoma identified mitochondrial one-carbon metabolism as a regulator of mTORC1-dependent autophagic degradation of TCF3,73 a finding consistent with our TCF3 reporter downregulation upon rapamycin treatment.