CALR and neoplasm: When subjected to excessive physicochemical or mechanical stress, tumor cells undergo an apoptotic state, prompting multiple events with the release of tumor-associated antigens (TAA) and the presentation of several damage-associated molecular patterns (DAMPs), such as increased exposure of the chaperone calreticulin (CRT), associated to a protein unfolding response, the release of high-mobility group box 1 (HMGB1), and adenosine triphosphate (ATP) secretion, eliciting an immunomodulatory activity and long-lasting immune response [16,17,18,19,20,21].