This critical role is further supported by the observation that Lyg1-deficient mice exhibit accelerated tumor progression, accompanied by reduced T cell numbers and impaired IFN-γ production.​ LYG1 deficiency also attenuates the severity of acute graft-versus-host disease (aGVHD) by skewing allogeneic T cells toward regulatory T cells (Tregs), along with decreased expression of activation markers (e.g., CD69) and pro-inflammatory cytokines (e.g., IFN-γ) in T cells (6). This evidence concerns the gene LYG1 and graft versus host disease.