DNA repair mechanisms such as HR and TLS were shown to protect against CFS breakage, presumably by promoting fork restart, and repair proteins such as 53BP1, ATR, RECQ1 have been found to be localized to CFS in response to replication inhibition by aphidicolin, an experimental method of accentuating fork stalling at CFS (47,48,51). This evidence concerns the gene RECQL and myalgic encephalomeyelitis/chronic fatigue syndrome.