BCL2L1 and Thrombocytopenia: In line with these observations, an independent approach showed that genetic ablation or pharmacological inactivation of Bcl-xl reduces platelet half-life and causes thrombocytopenia in mice.34 The central role of Bcl-xl in malignant transformation of hematopoietic cells was further strengthened with the fact that transgenic mice overexpressing Bcl-xl developed lymphomas.35