Additionally, Zhao and coworkers found that the suppression of Bcl-xL deamidation by an oncogenic tyrosine kinase contributes to etoposide and γ-radiation resistance in a mouse tumor model [23] and in human myeloproliferative disorders [34], and there is evidence that suppression of Bcl-xL deamidation is a component of hepatocellular carcinogenesis [35]. The gene discussed is BCL2L1; the disease is myeloproliferative disorder.