One study showed that in prostate cancer cells, TPL-based drugs stimulated the release of free calcium, promoted endoplasmic reticulum stress and induced activation of the CAMKKb-AMPK signaling pathway, leading to inhibition of mTOR and activation of beclin-1 and Unc-51-like kinase 1 (ULK1), thereby promoting autophagy.91 Currently, a clinical trial has investigated the safety and anticancer efficacy of the TPL derivative F60008 in patients with advanced solid tumors. Here, ULK1 is linked to prostate carcinoma.