EGFR and breast carcinoma: USP43 thus robustly suppresses breast cancer growth and metastasis.[156] In breast cancer, USP43 can be phosphorylated on Ser29 by activated AKT and sequestrated in the cytoplasm through interacting with the 14‐3‐3β/ε heterodimer.[156] Decreased nuclear USP43 leads to EGFR upregulation, which further strengthens the EGFR/PI3K/AKT pathway to accelerate breast cancer progression.[156] BAP1 deubiquitinates PTEN and stabilizes it, which allows PTEN to negatively mediate AKT kinase activity.