The RAD51-independent ALT-like mechanism in human cancer is considered the dominant mechanism of telomere lengthening during the G2/M phase, which facilitates RAD52-dependent BIR for telomere synthesis and requires BLM for resolving BIR intermediates, recruiting RAD52 and other DDR proteins to APBs, and generating replication stress [72]. This evidence concerns the gene RAD52 and cancer.