A recently published study revealed the essential role of TIA1 and TIAL1 in promoting the survival of GC B cells by regulating the expression of the prosurvival protein MCL1 [10]. These findings provide valuable insights into the role of TIA1 and TIAL1 in driving GC B cell responses and shaping the processes underlying the critical role of RBPs in regulating B cell fate after affinity maturation (Fig. 1). To understand the function of TIA1 and TIAL1 in GC B cells, the authors generated mice with conditional knockout of TIA1 and TIAL1 and found that the generation of antigen-specific GC B cells was severely impaired in Tial and Tial1 double knockout (dKO) mice compared to control mice. Consistent with this finding, the production of high-affinity antibodies, especially IgG1 homologous antibodies, induced by the thymus-dependent antigen NP-KLH was significantly reduced in mice lacking TIA1 and TIAL1.