This observation was further validated by injecting CD117+CD82+ T-ALL cells into immune-deficient mice at limiting dilution and finding enrichment in the leukemia-initiating capacity in this population of cells in two independent primary T-ALL samples.64 Taken together, these findings imply that the LSC activity in T-ALL might originate from different subpopulations of cells and underscore the heterogeneity within LSCs. Here, CD82 is linked to acute lymphoblastic leukemia.