Evaluation of its efficacy into IK, AN3CA, and HEC-1A endometrial cancer cell lines showed that ABTL0812 reduced cell viability, promoted the activation of the pro-apoptotic pathway and autophagy induction by TRIB3 overexpression (a negative regulator of AKT1) promoting downregulation of mTOR resulting in autophagy activation (Figure 1) and the transformation of soluble LC3 (LC3-I) to a lipidated form (LC3-II) (38). Here, AKT1 is linked to endometrial cancer.