In context with FGFR1 overexpression-mediated activation of Akt and Erk1/2 [Figures 2 and 5], these data demonstrate that FGFR1-induced ERα phosphorylation and crosstalk between RTK-ER pathways are key mechanisms of alpelisib resistance in breast cancer cells. This evidence concerns the gene AKT1 and breast carcinoma.