The estrogen receptor (ER) is a validated target for the treatment of estrogen receptor- positive (ER+) breast cancer. In recent years ER degraders based on the proteolysis targeting chimeras (PROTAC) have been developed. The aim of this paper is to justify through computational means the success or failure of some of these molecules and suggest improvements. An initial focus is placed on the kinetics of ternary complexes and the possibility that, unlike traditional occupancy-based pharmacology, in PROTAC design a higher affinity for the targets does not suggest a more effective result. Furthermore, computational methods are used to analyze the behavior of PROTACs targeting Estrogen Receptor when the linker composition is changed.