Gimap3 (IAN4) and Gimap5 (IAN5) are highly homologous GTP‐binding proteins of the Gimap family. Gimap3 and Gimap5, whose transcripts are abundant in mature lymphocytes, can associate with antiapoptotic Bcl‐2 family proteins. While it is established that Gimap5 regulates T‐cell survival, the in vivo role of Gimap3 is unclear. Here we report the preparation and characteristics of mouse strains lacking Gimap3 and/or Gimap5. We found that the number of T cells was markedly reduced in mice deficient in both Gimap3 and Gimap5. The defects in T‐cell cellularity were more severe in mice lacking both Gimap3 and Gimap5 than in mice lacking only Gimap5. No defects in the cellularity of T cells were detected in mice lacking only Gimap3, whereas bone marrow cells from Gimap3‐deficient mice showed reduced T‐cell production in a competitive hematopoietic environment. Moreover, retroviral overexpression and short hairpin RNAs‐mediated silencing of Gimap3 in bone marrow cells elevated and reduced, respectively, the number of T cells produced in irradiated mice. These results suggest that Gimap3 is a regulator of T‐cell numbers in the mouse and that multiple Gimap family proteins cooperate to maintain T‐cell survival.