The low numbers of patients with mutations or amplifications in CDK9 for most cancers (Figure 5), a key feature that helped in selectively targeting other kinases like BRAF (Vemurafenib and Dabrafenib against BRAFV600E) and MEK1/2 (Trametinib against BRAFV600E/K) specifically in cancer cells [165,166], probably also affected the effectiveness of the next generation inhibitors, which targeted CDK9 far more selectively. This evidence concerns the gene CDK9 and cancer.