Recent strategies of targeting c-Myc indirectly, such as with BRD4 or CDK7 inhibitors showed a therapeutic window for targeting c-Myc, alleviating the above concerns (53, 54).Han et al. developed the c-Myc inhibitors with well tolerability that disrupted MYC/MAX heterodimerization, enhanced c-Myc degradation, and impaired c-Myc-driven gene expression to increase tumor immune cell infiltration, and sensitize tumors to anti-PD1 immunotherapy (27). This evidence concerns the gene MAX and neoplasm.