60 In recent years, a significant debate has emerged within the medical community regarding the classification of chronic myeloid leukaemia (CML). Specifically, experts are divided on the existence of an accelerated phase in the progression of this blood cancer. This controversy has profound implications for diagnosis, treatment, and patient outcomes, prompting renewed scrutiny and research into the biological and clinical aspects of CML. The findings were published in the journal Leukemia. CML, a type of cancer that affects the bone marrow and blood, has traditionally been classified into three phases: chronic, accelerated, and blast. The chronic phase is characterised by an overproduction of mature white blood cells, while the blast phase is marked by a rapid increase in immature white blood cells (blasts). The accelerated phase is considered an intermediate stage, thought to signal a transition from chronic to blast phase. However, this classification has been called into question by recent studies and evolving clinical guidelines. The World Health Organization (WHO) in 2022 decided to eliminate the accelerated phase from its classification of myeloid neoplasms. According to the WHO, the designation of the accelerated phase has become less relevant in the context of modern treatment approaches, such as tyrosine kinase inhibitors (TKIs). These treatments target specific genetic abnormalities in cancer cells, effectively controlling the disease and reducing the incidence of progression to blast phase. The WHO’s decision is based on the understanding that resistance to TKIs and the development of additional cytogenetic abnormalities are the key factors in disease progression, rather than the presence of an accelerated phase. Biologically, there is evidence suggesting that chronic phase CML might be more accurately described as a preleukaemia rather than a true leukaemia. This is because the cells in chronic phase CML continue to differentiate normally, respond to physiological regulatory signals, and function mostly normally. There is no clear evidence of uncontrolled proliferation typical of cancerous cells in the chronic phase. Instead, the primary issue is an overproduction of cells that otherwise behave normally. From a clinical perspective, the concept of an accelerated phase was introduced before the advent of TKIs, based on the identification of certain laboratory and clinical features associated with a higher risk of progression to blast phase. However, with the effective control provided by TKIs, the relevance of these features has diminished. A study involving over 2,000 patients found that those classified as being in the accelerated phase had similar outcomes to those in the chronic phase when treated with TKIs, further questioning the utility of the accelerated phase classification. The controversy is not without its detractors. The European Leukemia Net (ELN) and the International Consensus Classification (ICC) continue to recognise the accelerated phase, citing its importance in risk stratification and treatment planning. They argue that certain patients exhibit clinical and laboratory features that clearly differentiate them from those in the chronic phase, warranting the intermediate classification. Additionally, the 2024 guidelines from the National Comprehensive Cancer Network (NCCN) also retain the accelerated phase, reflecting ongoing divergence in clinical practice. Despite these differing viewpoints, the push to redefine or eliminate the accelerated phase is gaining traction. Proponents of this change argue that the presence of high-risk features should instead be viewed as a spectrum of disease severity within the chronic phase rather than a distinct intermediate phase. This perspective aligns with the biological understanding that CML cells in the chronic phase resemble normal cells more closely than those in the blast phase. One of the main challenges in resolving this debate is the lack of consensus on the criteria defining the accelerated phase. Different guidelines and studies use varying thresholds and markers, leading to inconsistency in diagnosis and treatment. This inconsistency complicates clinical decision-making and underscores the need for a unified approach.