Considering that presumably, CALHM1 is exerting its cytotoxic effect during the reperfusion phase of brain ischemia, due to its activation properties (Ca2+ add-back protocol), we hypothesize that the absence of one allele of CALHM1 should be sufficient to reduce a large amount of Ca2+ influx into the neurons during the reoxygenation period, exerting a similar neuroprotective effect to the total ablation of CALHM1 gene. The gene discussed is CALHM1; the disease is brain ischemia.