To investigate the possible mechanism in KMT2A regulating VDAC1in promoting cell growth, we performed the rescued assay and found that overexpression of VDAC1 rescued the cell viability inhibition and cell apoptosis caused by KMT2A knockdown, revealing that VDAC1 signaling was involved in the KMT2A-mediated regulation of cervical cancer viability, cell migration and apoptosis. This evidence concerns the gene VDAC1 and cervical carcinoma.