In PCa, both granulocytic and monocytic MDSCs secrete reactive nitrogen species, such as nitrate lymphocyte‐specific protein tyrosine kinase in T cells, leading to a decline in T cell antitumor function in PTEN/P53/SMAD4 mouse models.[98] IL1β, a subtype of IL1, also affected the PCa immune TME.[99] Specifically, ADT enhances IL1β expression by suppressing AR function in MDSCs, which in turn attenuates the antitumor function of CD8+ T cells. The gene discussed is SMAD4; the disease is posterior cortical atrophy.