The stimulator of interferon genes (STING) is an adaptor protein involved in the innate immune response to the bacterial product cyclic dinucleotides (CDNs) or host DNA. The activation of STING pathway initiates interferon regulatory factor 3 (IRF3) and nuclear factor-κB (NF-κB). IRF3 can translocate to the nucleus and trigger the expression of immune stimulated genes (ISGs) and type I IFNs, leading to activation and migration of immune cells to the target cells, and NF-κB can drive the production of inflammatory cytokines. Thus, the activation of STING pathway may bridge innate and adaptive immunity. Autophagy, as an important part of cellular metabolism, is like a “smart recycling bin” in the human body, degrading abnormal and redundant substances and providing materials for the synthesis of new molecules to assist in maintaining homeostasis. Both STING and autophagy play a vital role in cellular, tissue, and organismal homeostasis. Due to the importance of STING and autophagy in maintaining cell survival and functional homeostasis, an increasing number of studies confirm that they are closely linked with each other. There are two main aspects: one is the regulation of autophagy key proteins by STING-dependent signaling network, the other is the regulation of autophagy on distinct links of STING activation pathway. Moreover, aberrant activation of STING or autophagic dysfunction, is critically involved in the pathogenesis of various illnesses, and more in-depth research has found that they jointly participate in the occurrence and development of diseases. This review will summarize the latest research on the mechanism of STING signaling and autophagy interaction and related human diseases, which may shed new light on the prevention and treatment of various diseases.