Interestingly, conditions that induce replicative stress and CFS instability (e.g., low/mild-dose APH) foster 53BP1-NB accumulation, while others that induce replicative stress but not CFS instability (e.g., hydroxyurea) are not significantly associated with an increase in 53BP1-NBs [29,91]. This evidence concerns the gene TP53BP1 and myalgic encephalomeyelitis/chronic fatigue syndrome.