The pathogenesis of acute myeloid leukaemia is a gradual heterogeneous process induced in the majority of cases by multiple genetic aberrations The latest evidence shows that different genetic lesions play specific roles in this process cooperate with each other and are repeatedly found in a specific hierarchical order In many cases frank leukaemia is preceded by the development of non-malignant clonal haematopoiesis which transforms into a neoplastic process by the generation of further mutations The successive accumulation of mutations then produces leukemic sub-clones which may even constitute phenotypically different cell populations with different sensitivity to therapy and relapse-inducing ability This article aims to provide a concise review of the latest data on the kinetics of acute myeloid leukaemia generation and relapse and also on the role of somatic mutations most frequently involved in these processes.