Several c-Myc inhibitors, including JQ1, 10058-F4, 10074-G5, and Omomyc, were developed for cancer therapy on the basis of their targeting of c-Myc transcription or the interaction between c-Myc and its partner protein Max, thereby blocking their heterodimerization and subsequent binding to the E-box of the Myc promoter, leading to inactivation of downstream target gene expression (Wang et al., 2014; Allen-Petersen and Sears, 2019). Here, MYC is linked to cancer.