AKT1 and breast carcinoma: Vis-à-vis the underlying molecular pathways of these drugs on cell viability, EMT progression, cell invasion, and colony formation of HER2-positive breast cancer cells, we assumed that HER2 inactivation in addition to PI3K/AKT and c-Jun N-terminal kinase (JNK) pathways could have major roles in regulating these events [50–54]; therefore, the expression patterns of HER2, AKT, and JNK1/2/3 were explored.