{'fraction_non_alphanumeric': 0.022292993630573247, 'fraction_numerical': 0.005573248407643312, 'mean_word_length': 5.758064516129032, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The journey of a thousand miles begins with 1 step.

This study has implications for both clinical and translational research. The pathophysiology of MDS has remained largely obscure for a long time. High-throughput DNA sequencing has identified the key somatic mutation drivers of this type of malignancy, including splicing factors, DNA methylation, chromatin modification, transcription regulation, DNA repair, and signal transduction. In 2016, the World Health Organization classification added germline predisposition to myeloid neoplasms. This change has helped reveal the relatively well-hidden world of germline mutations in apparently sporadic hematologic cancers associated with a spectrum of underlying conditions. However, the relative contribution of the germline genetic component to the pathophysiology of MDS, as well as its clinical implications, still needs to be elucidated. Indeed, some disorders seem to have high penetrance and strong clinical expressivity that raise clinical suspicion, whereas others, such as germline DDX41 mutations, do not. In addition, even within those mutations associated with organ dysfunction, clinical expression may be extremely variable, which results in late onset or incidental diagnosis in adulthood.