Endocrine resistance can be linked to numerous mechanisms of action, including upregulation of cyclin-dependent kinases (CDKs) 4/6, upregulation of phosphoinositide 3-kinase (PI3K)/AKT and mammalian target of rapamycin (mTOR) cell division signaling pathways, and estrogen receptor alpha (ESR1) gene mutation of the tumor ER [6]. Here, AKT1 is linked to neoplasm.