JAK2 and neoplasm: Since RelB-deficient diseased mice (both TEL-JAK2;Tcra−/−;Relb−/−mice and TEL-JAK2;Tcra−/−→Tcra−/−;Relb−/− chimeric mice) presented reduced thymic and lymph node tumor load compared to RelB-proficient controls, we conclude that defects in these organs were responsible for the delay in leukemogenesis.