MYC is extensively recognized as a proto‐oncogene, and its amplification is frequently observed in malignant tumors.[38] It has been reported that inhibition of this protein could result in the suppression of tumor growth.[39] Given that SadM‐CBE had a higher efficiency in the PAM‐proximal regions (Figure 8A), it was a promising tool to introduce a stop codon in MYC via base editing for oncogene disruption. Here, MYC is linked to cancer.