Acute Lymphoblastic Leukemia (ALL) in children is a highly treatable disease, with a cure rate of approximately 80%. The improvements in treatment outcomes are attributed to intensive multi-agent chemotherapy, the identification of predictive clinical and biological variables, advancements in supportive care, and large-scale clinical trials. Despite these successes, there is room for improvement, including better treatment for relapsed cases, less toxic therapies, and management of late effects. ALL is the most common childhood malignancy, accounting for 25% of all cancers in children and 72% of pediatric leukemias. It occurs at an annual rate of 3 to 4 cases per 100,000 children under 15 years old. The incidence peaks between 2 to 5 years of age, with males being more affected than females, except in infants. Geographic variations exist, with the highest incidence in industrialized Western countries and the lowest in North Africa and the Middle East. Maternal reproductive history, fetal loss, and increased in utero growth rates are linked to an increased risk of ALL. The pathogenesis of ALL involves the malignant proliferation of lymphoid cells at early stages of differentiation. Genetic factors play a significant role, with molecular techniques documenting the presence of leukemia-specific genetic abnormalities in neonatal blood. Postnatal oncogenic mutations may lead to clinically detectable leukemia. Environmental factors, including irradiation, certain chemicals, viral infections, and immunodeficiencies, also contribute to leukemogenesis. ALL is classified based on morphological, immunological, and genetic features. The FAB system categorizes lymphoblasts into L1, L2, and L3 types, with L1 being the most common in children. The WHO classification subdivides cases into precursor B-cell, precursor T-cell, and mature B-cell ALL. Genetic abnormalities, such as hyperdiploidy, trisomies, and Philadelphia chromosome, are important for diagnosis, risk assessment, and prognosis. Children with ALL often present with symptoms related to bone marrow infiltration and extramedullary disease spread. Initial symptoms may include anemia, thrombocytopenia, and neutropenia. Laboratory findings typically include elevated white blood cell counts, anemia, and thrombocytopenia. Bone marrow aspirates are necessary for definitive diagnosis. Prognostic factors include age at diagnosis, initial WBC count, sex, race, extramedullary disease, blast immunophenotype, cytogenetics, early response to therapy, and minimal residual disease (MRD). Children under 1 year and over 10 years of age have inferior prognoses. T-cell ALL and infants with t(4;11) have higher initial WBC counts. Girls generally have better prognoses than boys. Early responders have better outcomes, and MRD levels below 10^4 at the end of induction therapy are associated with the best prognosis.Acute Lymphoblastic Leukemia (ALL) in children is a highly treatable disease, with a cure rate of approximately 80%. The improvements in treatment outcomes are attributed to intensive multi-agent chemotherapy, the identification of predictive clinical and biological variables, advancements in supportive care, and large-scale clinical trials. Despite these successes, there is room for improvement, including better treatment for relapsed cases, less toxic therapies, and management of late effects. ALL is the most common childhood malignancy, accounting for 25% of all cancers in children and 72% of pediatric leukemias. It occurs at an annual rate of 3 to 4 cases per 100,000 children under 15 years old. The incidence peaks between 2 to 5 years of age, with males being more affected than females, except in infants. Geographic variations exist, with the highest incidence in industrialized Western countries and the lowest in North Africa and the Middle East. Maternal reproductive history, fetal loss, and increased in utero growth rates are linked to an increased risk of ALL. The pathogenesis of ALL involves the malignant proliferation of lymphoid cells at early stages of differentiation. Genetic factors play a significant role, with molecular techniques documenting the presence of leukemia-specific genetic abnormalities in neonatal blood. Postnatal oncogenic mutations may lead to clinically detectable leukemia. Environmental factors, including irradiation, certain chemicals, viral infections, and immunodeficiencies, also contribute to leukemogenesis. ALL is classified based on morphological, immunological, and genetic features. The FAB system categorizes lymphoblasts into L1, L2, and L3 types, with L1 being the most common in children. The WHO classification subdivides cases into precursor B-cell, precursor T-cell, and mature B-cell ALL. Genetic abnormalities, such as hyperdiploidy, trisomies, and Philadelphia chromosome, are important for diagnosis, risk assessment, and prognosis. Children with ALL often present with symptoms related to bone marrow infiltration and extramedullary disease spread. Initial symptoms may include anemia, thrombocytopenia, and neutropenia. Laboratory findings typically include elevated white blood cell counts, anemia, and thrombocytopenia. Bone marrow aspirates are necessary for definitive diagnosis. Prognostic factors include age at diagnosis, initial WBC count, sex, race, extramedullary disease, blast immunophenotype, cytogenetics, early response to therapy, and minimal residual disease (MRD). Children under 1 year and over 10 years of age have inferior prognoses. T-cell ALL and infants with t(4;11) have higher initial WBC counts. Girls generally have better prognoses than boys. Early responders have better outcomes, and MRD levels below 10^4 at the end of induction therapy are associated with the best prognosis.