By maintaining the stability of client proteins such as the AR, estrogen receptor (ER) and MYC, heat shock proteins modulate the activity of different pathways, including the PI3K/Akt, JAK/STAT3, PKL1 and MAPK pathways, eventually leading to uncontrolled cell growth, persistent angiogenesis, apoptosis evasion, tumor invasion and metastasis [26–28]. This evidence concerns the gene AR and neoplasm.