Our current findings show that B-DIM can activate AMPK signaling as early as three hours in both androgen-sensitive LNCaP and androgen-insensitive C4-2B prostate cancer cells, measured by: (i) increased protein levels of phosphor-AMPKα (T172), (ii) increased levels of phosphorylated ACC on serine residue 79 [30]–[31], (iii) increased protein levels of phosphor-Raptor (S792), which is a direct target of AMPK and an mTOR binding partner and inhibitor [8], and (iv) decreased levels of phosphor-mTOR (Fig. 1). The gene discussed is RPTOR; the disease is prostate carcinoma.