{'fraction_non_alphanumeric': 0.0267515923566879, 'fraction_numerical': 0.014012738853503185, 'mean_word_length': 5.661016949152542, '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}}
In this issue of Epigenetics

Single nucleotide polymorphisms in the vicinity of the INK4b-ARF-INK4a human locus, which encodes for two cyclindependent kinase inhibitors with wellestablished tumor suppressor functions and a regulator of the p53 pathway, are linked to a wide spectrum of conditions, including cardiovascular disease, ischemic stroke, type 2 diabetes, frailty, and Alzheimer’s disease. The INK4b-ARFINK4a locus is regulated by Polycomb repressive complexes, which interact with other epigenetic modifiers such as histone demethylases JMJD3 and JHDM1B, the SWI/SNF chromatin remodeling complex, and DNA methyltransferases. In this issue of Epigenetics, Popov and Gil review aspects of the epigenetic regulation of the INK4b-ARF-INK4a locus and its involvement on disease.