Figure 2: Schematic representation of the mechanisms involved in the maintenance of stability at common fragile sites. After replication, inhibition DNA secondary structures are formed within CFS leading to fork stalling. The replication checkpoint is triggered, and several proteins were recruited to recover stalled forks. Among the proteins involved in the safe resumption of replication forks are FANCD2 and WRN helicase. However, in case of failure checkpoint activation or in absence of key proteins, chromosomal abnormalities take place giving rise to genome instability (see text for details).