Intermittent fasting (IF), which is also called fasting on a schedule or a fasting-mimicking diet (FMD), has been found to be beneficial for health by reducing risk factors and reversing symptoms of serious health conditions, including cancer. Although the mechanisms behind these beneficial effects of IF are not clearly understood, several potential mechanisms have been suggested. Overall, IF is associated with the conversion of the energy metabolic response from glucose to ketone bodies as an energy source, enhancing ketone body production, autophagy, DNA repair, anti-stress abilities, and antioxidant defense. In tumor cells, these events result in the inhibition of the IGF-1/AKT and the mammalian target of rapamycin (mTORC1) pathways and increase adenosine monophosphate (AMP)-activated protein kinase (AMPK), which is dependent on the sirtuin-1 (SIRT1) and SIRT3 pathways. These molecular cascades can hinder tumor cell growth. Furthermore, in cancer cells, IF alters autophagy, which is a conserved lysosomal degradation pathway for the intracellular recycling of macromolecules and clearance of damaged organelles and misfolded proteins to ensure cellular homeostasis. IF can also increase the sensitivity of cancer cells to chemotherapy and radiotherapy; it can also reduce the side effects of conventional anticancer treatments. Further, IF can influence gene expression regulation by acting on certain types of microRNAs (miRNAs). Most importantly, IF can enhance the quality and quantity of both innate and adaptive immune cells by triggering stem cells to regenerate the immune system, as well as by increasing the production of tumor-killing immune cells, thereby inhibiting tumor growth and improving antitumor immune responses. Given these beneficial effects of IF, it is recommended to use fasting as an adjuvant therapy for cancer treatment, including immunotherapy.