The hyperactivation of intracellular signalling pathways is a hallmark of cancer cells which can be due to a variety of causes: mutations or chromosomal rearrangements targeting tyrosine kinases (TK) such as FLT3, KIT or BCR::ABL1 alterations in hematologic malignancies; indirect mechanisms such as HER2 TK receptor overexpression in breast cancers; mutations in PI3K/AKT or RAS signalling pathways in many cancer subtypes. This evidence concerns the gene ABL1 and breast carcinoma.