ATM (ATM serine/threonine kinase) is a serine/threonine protein kinase that functions as a critical DNA damage sensor, activating checkpoint signaling upon double-strand breaks (DSBs) and genotoxic stresses such as ionizing radiation and ultraviolet A light 1. The kinase recognizes substrate consensus sequences containing [ST]-Q motifs 1 and phosphorylates numerous DNA repair and signaling proteins including p53, CHEK2, BRCA1, and H2AX, thereby regulating DNA damage response mechanisms 1. ATM coordinates multiple cellular processes beyond DNA repair, including pre-B cell allelic exclusion through repositioning of immunoglobulin alleles to pericentromeric heterochromatin, preventing recombination of non-selected alleles [UniProt]. The kinase also participates in signal transduction, cell cycle control, and replication-dependent histone mRNA degradation [UniProt]. Additionally, ATM mediates pexophagy by phosphorylating PEX5 in response to reactive oxygen species, promoting peroxisome selective autophagy 2. Biallelic mutations in ATM cause ataxia-telangiectasia, a severe immunodeficiency disorder characterized by neurodegeneration, cancer predisposition, and radiosensitivity, establishing ATM as a critical tumor suppressor [NCBI/UniProt]. ATM's multifaceted roles in genomic stability maintenance make it essential for cellular homeostasis and cancer prevention.