Clinically, specific subtypes of this cancer are based primarily on their histopathological appearance and expression of estrogen receptor (ER), progesterone receptor (PR), and ERBB2 receptor (HER2).56 A pan-cancer analysis revealed that Parkin is frequently deleted in breast cancer (32% deletion rate).50 Cancer-specific alteration of Parkin abrogates its tumor-suppressive function for the involvement of this E3 Ub ligase in proteasomal degradation of cyclin D and cyclin E, which subsequently control cell cycle progression. This evidence concerns the gene ESR1 and neoplasm.