For instance, p53/nf1-deficient fish were used by Oppel et al. to knock out by CRISPR/cas9 the atrx gene, a known tumor suppressor in gliomas or sarcomas, confirming that its loss facilitates the development of various malignancies, together with the downregulation of telomerase, which causes the alternative lengthening of telomeres [86]. The gene discussed is TP53; the disease is neoplasm.