In a complementary approach, querying TCGA dataset allowed us to determine clinically meaningful factors, and thus we found MYBL2 expression was also upregulated and correlated with A3B expression in breast and multiple cancer types, implying that B-Myb might act as a general transcription factor for A3B induction, and MYBL2 upregulation could explain how A3B is upregulated in multiple human cancers. The gene discussed is MYBL2; the disease is cancer.