Therefore, we suggest that the ATAD2‐related cancer stem cell‐like phenotype is mediated through both ATAD2 and c‐Myc proteins and propose ATAD2 as a druggable target for de‐differentiated tumors (especially those overexpressing MYC), which emerges achievable when considering its ATPase activity and its bromodomain. This evidence concerns the gene MYC and cancer.