Acute lymphoblastic leukaemia (ALL) occurs in both children and adults. However, the median age at initial diagnosis is 15 years and more than 50% of newly diagnosed patients are less than 20 years old [1,2]. B-cell precursor acute lymphoblastic leukaemia (B-ALL) is the most common pediatric malignancy accounting for up to 20% of all cancers diagnosed in children, and up to 80% of all pediatric ALL cases [3]. Over decades, pediatric ALL has become an exemplary model of successful cancer treatment, as demonstrated by gradual improvement in survival rates, reaching 90% in modern treatment protocols [[4], [5], [6], [7], [8], [9], [10], [11], [12]] [[4], [5], [6], [7], [8], [9], [10], [11], [12]] [[4], [5], [6], [7], [8], [9], [10], [11], [12]]. This increase in survival can be explained by introduction of multidrug treatment regimen in structured clinical trials in the 1960's [5,13], as well as the introduction of the first risk-addapted treatment protocols, based on clinical and cytogenetic parameters, in the 1970's [[14], [15], [16], [17]]. Risk stratification of patients based on their clinical, cytogenetic and molecular characteristics proved to be a successful strategy in the following decades, becoming increasingly complex with advances in cytogenetic techniques such as karyotyping, fluorescent in situ hybridization (FISH) and DNA microarrays. Furthermore, improvements in molecular genetics technology, including the introduction of next generation sequencing (NGS) approaches, have resulted in the discovery of novel genetic alterations [[18], [19], [20], [21], [22]], and paved the way for the introduction of novel targeted therapy in leukaemia treatment, e.g., second and third generation tyrosine kinase inhibitors (TKI) for the treatment of Philadelphia-positive leukaemia resistant to first generation TKI (imatinib) [23], and, more recently, the development of immunotherapeutic approaches [24].