DNA double strand breaks (DSBs) are highly toxic to the cells and accumulation 
of DSBs results in several detrimental effects in various cellular processes 
which can lead to neurological, immunological and developmental disorders. 
Failure of the repair of DSBs spurs mutagenesis and is a driver of 
tumorigenesis, thus underscoring the importance of the accurate repair of DSBs. 
Two major canonical DSB repair pathways are the non-homologous end joining 
(NHEJ) and homologous recombination (HR) pathways. 53BP1 and BRCA1 are the key 
mediator proteins which coordinate with other components of the DNA repair 
machinery in the NHEJ and HR pathways respectively, and their exclusive 
recruitment to DNA breaks/ends potentially decides the choice of repair by 
either NHEJ or HR. Recently, Rap1 interacting factor 1 has been identified as an 
important component of the DNA repair pathway which acts downstream of the 
ATM/53BP1 to inhibit the 5'-3' end resection of broken DNA ends, in-turn 
facilitating NHEJ repair and inhibiting homology directed repair. Rif1 is 
conserved from yeast to humans but its function has evolved from telomere length 
regulation in yeast to the maintenance of genome integrity in mammalian cells. 
Recently its role in the maintenance of genomic integrity has been expanded to 
include the regulation of chromatin structure, replication timing and intra-S 
phase checkpoint. We present a summary of these important findings highlighting 
the various aspects of Rif1 functions and discuss the key implications for 
genomic integrity.