The treatment of ERBB2-amplified breast tumor cells with the ErbB2-specific antibody trastuzumab causes cell cycle arrest accompanied by a decrease in PI3K/Akt activity and the downregulation of c-MYC and D-type cyclins; on the other hand, ectopic expression of c-MYC in ERBB2-overexpressing SKBr3 cells partially rescues the cells from functional ERBB2 inactivation [3,4]. This evidence concerns the gene MYC and breast neoplasm.