Very recently, it has been reported that overexpression of the BCR-ABL fusion oncogene and other tyrosine kinases in leukemia leads to overexpression of DNA polymerase theta (DNA Pol θ) and accumulation of DNA–protein crosslinks (DPCs) containing DNA double-strand breaks by POLθ-mediated end-joining; inhibition of this polymerase can help eradicate BCR-ABL-positive stem cells [39,40]. The gene discussed is BCR; the disease is leukemia.