Concluding, the assessment of the levels and activities of CCS proteins and our successful attempt to modulate their activity leading to the induction of blast apoptosis may help to understand the pathomechanism of ALL better; it may also contribute to the development of new prognostic markers and possibly therapeutic strategies, where μ-calpain, and/or perhaps calpastatin may become potential targets for new (supplementary) anti-ALL therapy. The gene discussed is CAST; the disease is acute lymphoblastic leukemia.