Furthermore, there was a lower proportion of activated cells (CD62LloCD44hi) among both CD4+ and CD8+ T lymphocytes in FABP4 knockout mouse spleens and decreased IFN‐γ‐ and TNF‐α‐producing T lymphocytes, which may be the reason why FABP4 deficiency protected mice from STZ‐induced T1D development. This evidence concerns the gene CD8A and type 1 diabetes mellitus.