Consistent with previous reports, we found that citrate treatment in tumor cells modulate ATM‐associated DNA damage, activates ERK1/2 and p38 MAPK, and mTOR signaling pathways during tumor cell senescence development.[31, 32, 33] In addition, ATM‐associated DDR cooperates with MAPK and mTOR signing pathways to control hyper‐activation of lipid metabolism, which results in tumor cell senescence and growth inhibition.[29, 31, 32, 33, 34, 43, 52] Collectively, our studies have identified the mechanistic basis for the development of citrate as a therapeutic target for tumor treatment. Here, MTOR is linked to neoplasm.