The development of cancer immunotherapies provides hope to millions of patients for better clinical outcomes after tumor treatment. Thus, investigating the fundamental mechanisms of antitumor immunity activation is an urgent task. Numerous studies have outlined the effect of immunogenic cell death (ICD) on cancer cells, and this outcome is both sophisticated and simple. Different stimuli can cause ICD; however, photodynamic exposure has been proven to be an effective inducer of programed death on par with radiotherapy. The link between triggering a photodynamic response in cancer cells and triggering ICD has been poorly described in experimental works. The question of which molecular cascades are activated after photodynamic therapy (PDT) irradiation and the way damage-associated molecular patterns (DAMPs) are released is intriguing. Much is known about reactive oxygen species generation and endoplasmic reticulum stress but little about the Golgi apparatus. Photosensitizers of different types can exert different effects, including completely nonimmunogenic ones. This review describes the cascades that link the induction of cell death by photodynamic exposure and the immunogenic pattern of DAMP release. The photosensitizers that have shown potential as ICD inducers and the different pathways of programed death that occur during PDT exposure are also discussed.