Moreover, using a 3D phenotypic reversion assay, Lee et al.19 identified that FAM83A may contribute to resistance to tyrosine kinase inhibitors in breast cancer through activation of the epidermal growth factor receptor/phosphatidylinositol 3 kinase/AKT signaling pathway via interacting with c-RAF and phosphatidylinositol 3 kinase p85,20 indicating that overexpression of FAM83A may lead to chemoresistance. The gene discussed is SACK1A; the disease is breast carcinoma.