Following the knockdown of ID4 in LNCaP cells [L(−)ID4], increased protein stability along with the constitutive activation of androgen receptor marked by increased AR‐dependent expression including PSA, FKBP51, and ARD1 as well as ability to interact with the androgen response elements of the respective androgen‐responsive genes such as PSA, FKBP51, TMPRSS2, and ETV1 unequivocally supports the tumor suppressor role of ID4 in the regulation of AR expression and activity. The gene discussed is TMPRSS2; the disease is neoplasm.