The human BCL2 with amino acids 101-103 mutated from glycine-aspartate-aspartate to alanine-alanine-alanine to abolish BH3 domain pro-apoptotic function is under the control of the T cell-specific Cd4 locus control region (LCR). Immunohistochemistry confirmed expression of the transgene in thymocytes. A compensatory downregulation of endogenous mouse Bcl2 in the thymus, lymph nodes, and spleen is seen with transgene expression. Two lines were chosen for analysis, A and B, with similar phenotypes.