Telomere length is regulated around an equilibrium set point. Telomeres shorten 
during replication and are lengthened by telomerase. Disruption of the length 
equilibrium leads to disease; thus, it is important to understand the mechanisms 
that regulate length at the molecular level. The prevailing protein-counting 
model for regulating telomerase access to elongate the telomere does not explain 
accumulating evidence of a role of DNA replication in telomere length 
regulation. Here I present an alternative model: the replication fork model that 
can explain how passage of a replication fork and regulation of origin firing 
affect telomere length.