The abscopal effect (AE) induced by radiotherapy (RT) can inhibit tumor growth outside of the radiation field, and it was defined as a systemic antitumor response generated by local RT. At present, preclinical and clinical studies have reported that conventional RT rays (X-rays and γ-rays) could lead to immunogenic cell death (ICD) and the release of immunostimulatory factors from irradiated tumor cells, which include tumor-associated antigens (TAAs) and damage-associated molecular patterns (DAMPs). These factors recruit and activate dendritic cells (DCs) and then activate CD8⁺T cells to become cytotoxic T cell lymphocytes (CTLs). As a result, CTLs kill primary tumors as well as non-irradiated tumor metastases. However, the mechanism of the AE induced by RT is extremely complicated, and there are fewer studies on the roles of macrophages, p53, and exosomes in radiation-induced AE. In addition, compared with conventional RT, carbon ions beam has the advantages of high linear energy transfer (LET), high relative biological effectiveness (RBE), low oxygen enhancement ratio (OER), complex DNA damage, and the potential to activate stronger immunogenicity of tumor cells. Moreover, the mechanism of the AE induced by carbon ions radiotherapy (CIRT) is unclear. This article summarizes the complex molecular mechanisms of AE induced by conventional RT and CIRT, and elucidates the difference between the two radiation types. We found CIRT may lead to increased DAMPs released from irradiated tumor cells, and enhance the inhibition of tumor cell metastasis compared with conventional RT. We therefore propose that CIRT can induce a stronger AE than conventional RT. This article provides a theoretical basis for finding more effective radiotherapeutic approaches in the future.