AML is defined as a clonal disease that alters the progression of progenitor myeloid cells due to a loss in differentiation, cell cycle regulation, and apoptosis, thus allowing unlimited self-renewal. These alterations are based on genetic mutations that can disconnect the cell of origin from the normal pathways of its cycle and metabolism, giving leukemic cells an ability to adapt to the environment; altering their metabolism, which can confer resistance to treatment and evasion of the immune response. Within these leukemic cells, it is known that there are cells that can maintain their cell cycle in total quiescence, which, according to what makes it possible to clarify their proliferative capacity once they find the adequate medium to replicate, and explains the leukemogenic capacity of these leukemic cells. On the other hand, it has been observed that the most notable change in these cells at the metabolic level is the increase in glycolytic metabolism, an increase in the production of mitochondrial ATP in a defective way and the expression of a series of factors that promote resistance to chemotherapy conventional. These cells are also involved in primary and secondary refractoriness to treatment, associated with an earlier relapse time, an increase in minimal residual disease, and a decrease in their overall survival rate. In the same way, there is a direct association with the functional change of these leukemic cells; genetic mutations. For mutations it has been observed that great heterogeneity can be found and usually up to 5 mutations are identified at the same time and at least 1 mutation will be found in AML. The genes that are commonly altered are RUNX1, NPM1, P53, DNMT3a, SRSF2 and SF3B1 and FLT3; However, we can also find cytogenetic mutations such as the translocations t (8; 21) (q22; q22) and inv (16) (p13; q22), t (15; 17) (q24; q21), among others. That is why one of the most important determinants for the diagnosis and evaluation of progression is flow cytometry, which allows evaluating markers involved in differentiation, maturation and their relationship with the genetic mutation of the tumor. Also the analysis of the immunophenotype versus normal cells can help us to determine the risk of relapse, the resistance after chemotherapy and together with the evaluation of the minimal residual disease that is one of the most important prognostic values. Although studies have already been described at a global level of the relationship of immunophenotypic markers, genetic, cytogenetic and molecular traits, it is expected to be able to apply the relationship between immunophenotype with prognostic impact variables and outcome in Colombian patients of the San Ignacio University Hospital that allow us to identify together with diagnostic tools for patients with a higher risk of relapse, refractoriness to therapy and risk of death.