Downregulation of KMT2A was further shown to suppress cervical cancer cell proliferation and migration, accompanied with an activation of PARP/Caspase pathway and inhibition of VADC1, whereas overexpression of VDAC1 leads to a reversal of the KMT2A knockdown mediated changes, indicating that KMT2A/VDAC1 signaling axis might be a new therapeutic target for cervical cancer prevention.416. The gene discussed is VDAC1; the disease is cervical cancer.