Autophagy and apoptosis are two important life processes that share similar protein components, play essential role in the survival and development of the organisms and especially cancers. During the development of cancer, the two processes can trigger simultaneously with a delicate and complex relationship. Tumor suppressor Ras association domain family 1A (RASSF1A) is an important downstream effector of Ras superfamily proteins. RASSF1A is widely expressed in human tissues but is down-regulated in a variety of tumor cells due to its promoter methylation and transcription inhibition. Recent studies have shown that RASSF1A can regulate both apoptosis and autophagy through multiple pathways upon different cancer cellular state. In this article, we mainly review the regulatory mechanism of RASSF1A on autophagy through the mTORC1 signaling pathway, microtubule stability, and Rho subfamily proteins, and the regulatory mechanism of RASSF1A on apoptosis through MOAP1 proteins, or the Hippo pathway, or DNA damage pathway. As different kinases phosphorylate RASSF1A to convey different "mantras" and thus stimulate different biological functions, we also analyze the role of post-translational modification in the functional switching of RASSF1A in regulating autophagy and apoptosis. Although RASSF1A can alter the nuclear localization of the downstream effector YAP, a core effector of the Hippo signaling, the phenotypes presented are largely distinct in different tumors. These observation further suggest that therapeutic strategies using demethylation alone are not applicable to all RASSF1A-methylated tumors. Therefore, in-depth investigation of the regulatory mechanism of RASSF1A in autophagy, apoptosis and cancer cell fate determination is of great significance in providing more precise and effective treatment strategies for tumor patients.