Time-restricted eating (TRE), which limits the daily meal timing to a window of 6-12 h, has been shown to reduce the risks of cardiometabolic diseases through consolidating circadian rhythms of metabolism and physiology. Recent advances indicate that canonical circadian clocks are dispensable for the actions of TRE in the liver, and that meal timing entrains circadian rhythms in peripheral tissues in a tissue-specific manner (e.g., the liver and fat are readily entrainable, whereas the heart and kidneys are resistant). Here, we propose that TRE engages clock-modulated checkpoints (CCPs) to reset circadian rhythms of tissue functions. Elucidation of CCPs would reveal the mechanistic basis of tissue responsiveness to TRE, and facilitate the use of TRE in precision medicine for cardiometabolic diseases.