Several mechanisms have been called into account to explain resistance to therapies, such as androgen receptor (AR) gain-of-function mutations or splice variants (e.g., AR-V7), loss of tumor suppressor genes (e.g., p53, pTEN), and modifications of stromal components into the tumor microenvironment, promoting invasion, neoangiogenesis, and metastatisation process [3]. The gene discussed is TP53; the disease is neoplasm.