However, under DNA damaging conditions and in cancers, the splice variants like MDM2-ALT1 and MDMX-ALT2, or other splice variants as discussed above, interact with and cause altered activity of endogenous MDM2 and MDMX leading to the stabilization of p53 and also act to fine-tune p53 transcriptional activity (Fig 5B). This evidence concerns the gene TP53 and cancer.