In TEL+ cells, hTR, along with its chaperone proteins including NHP2, associates with hTERT to form the functional telomerase holoenzyme complex. At ALT telomeres, ATR kinase activity mitigates recovery of stalled replication forks via fork regression and repair. Likely through its previously reported interaction with KU subunits, hTR expression in ALT+/hTR- cells induces the removal of RPA from telomeres by the DNA-PK/hnRNPA1 complex. The reduced RPA-p-RPAS33 abundance at ALT telomeres, in turn, reduces RAD51 recruitment and increases replication fork collapse events. These collapsed forks provide the substrate for break-induced telomere synthesis that concomitantly leads to POLD3-dependent C-circle production. If left unrepaired, collapsed forks can be further marked by 53BP1 in a process regulated by NHP2. Finally, hTR has a second important non-canonical, anti-apoptotic function as previously described (Gazzaniga & Blackburn, 2014), in both TEL+ and ALT+ cell lines. 