TF activity is altered in numerous cancer types in various ways, including by gene mutation (e.g., p53), deletion and amplification (e.g., c‐Myc), chromosomal translocation (e.g., MLL‐ELL), alteration of expression (e.g., TAL1), modifications such as phosphorylation (AP‐1), and nuclear sublocalization (NFκB).[4] In addition to these ways, we show here that TF activity is also controlled by AS. The gene discussed is KMT2A; the disease is cancer.