Among these, RAD51 is a protein encoding gene that is recruited to the perturbed replication DSBs and forks sites and respectively blocks the exonuclease activity of MRE11 on DSB repair and on the replicated genome and eventually limit self-DNA accumulation in the cytosol, this process also prevents the initiation of innate immune signaling mediated by STING (26), which brought an insight to the potential relationship between stemness and immune escape mechanisms in the tumor cell. The gene discussed is MRE11; the disease is neoplasm.