This is particularly relevant because it is commonly accepted that ALL is triggered by fusions (such as BCR-ABL1, ETV6-RUNX1 or those involving KMT2A) resulting from chromosomal rearrangements23, or by lesions affecting transcription factors (such as PAX5 P80R)16, but there is no clear evidence that gain-of-function mutations in signaling-related genes can initiate ALL. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.