During irradiation intervals, surviving tumor cells potentially resume accelerated proliferation and eventually repopulate the tumor.[3] Multiple mechanisms of repopulation have been elucidated, such as hypoxia, cancer stem cells (CSCs), etc. We have reported that radiation‐induced apoptotic cells can stimulate proliferation of survived tumor cell via caspase‐3/ca2+‐independent phospholipase A2/arachidonic acid/prostaglandin E2 paracrine pathway.[4] However, much remains to be figured out about the subset of tumor cells capable of repopulating and the key molecular mechanisms involved. The gene discussed is CA2; the disease is neoplasm.