In addition, evidence in hormone receptor positive (HR+) breast cancers suggest potential roles for upstream receptor overexpression (FGFR2) and de novo mutations in RAS, AKT1, AURKA, CCNE2, and/or ERBB2 in the activation of ERK following acquired CDK4i/6i resistance [24]. This evidence concerns the gene FGFR2 and breast carcinoma.