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While data availability is crucial in determining phenotypes, especially for NDDs, recent epidemiological cohorts provided convenient starting points

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Moreover, classical methylation changes in lung cancersuch as silencing of tumor suppressors p16 and RASSF1Afurther illustrate the importance of aberrant DNA methylation in tumorigenesis [71,72,73,74,75].Together, these observations support the notion that shared methylation-regulated pathways, exemplified by KCNK3, may underlie the molecular crosstalk between hypertension and lung cancer