FOXA1 and neoplasm: The mechanisms underlying endocrine resistance are highly complicated, involving mutations affecting various genes (such as ER, aromatase, and tyrosine kinase receptor) and signaling pathways (such as phosphatidylinositol 3-kinase and mitogen-activated protein kinase), variations in transcription factors (such as MYC, FOXA1, CTCF, or TBX3), epigenetic changes, metabolic reprogramming of tumor cells, or tumor microenvironment changes10.