The assay monitors KAP-1 phosphorylation as a readout for ATM-like activity using an AlphaLISA assay. The study aims to identify small molecules that can compensate for the loss of ATM in cells derived from A-T patients, a disease characterized by neurological symptoms, telangiectasias, primary immunodeficiency, marked sensitivity to ionizing radiation, chromosomal instability, and predisposition to cancer. The underlying genetic cause of A-T is null mutations in the ATM gene, which functions as a master regulator of the cellular response to double-strand breaks in DNA. Is the molecule effective to this assay?