ALL constitutes a variety tumors of lymphoid precursors, and may be separated as a first pass into those derived from B cell or T cell precursors.  ALL is also subclassified on the basis of genetic lesions that produce leukemias with different prognosis: For example, the ETV6-RUNX1 translocation is common in children and associated with an excellent prognosis, while BCR-ABL1 (Ph+) ALL is relatively more common in adults and associated with poor outcome, though this has been improved by therapy with tyrosine kinase inhibitors.  Other types of ALL may be defined on the basis of chromosome number: hyperdiploid ALL has a good prognosis and hypodiploid ALL a poor outcome.  Recently, important new subtypes of ALL have been identified.  BCR-ABL-like ALL has a gene expression profile similar to that of Ph+ALL; some have translocations involving kinases amenable to TKI therapy, while another subset has translocations involving the CRLF2 gene which upregulates CRLF2, detectable by flow cytometry.  Other new entities include iAMP21, a poor prognosis leukemia seen in children, as well as a form of hypodiploid ALL associated with a constitutional, rather than a somatic TP53 deletion. More recently, other forms of ALL with a distinct gene expression profile have been shown to be associated with unique translocations and differing prognoses; while not yet incorporated in the WHO classification, they are candidates for inclusion in the future. T-ALL does not have many subgroups, but early T precursor ALL is one defined by flow cytometry; this historically had a poor prognosis but optimal therapy overcomes it.