Previously it has been shown that CML patients with a higher tumor burden had lower levels of T cells directed towards the junction of the Bcr/Abl protein compared to patients with lower tumor burden [54] implicating that the Bcr/Abl junction is immunogenic and that a low tumor burden can stimulate an immune response while high tumor burden on the other hand may suppress T cells, possibly by membrane bound or secreted factors. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.