Mechanistically, this process is first initiated by therapy-induced tumor immunogenic cell death (ICD), usually characterized by three hallmark markers: exposure of an endoplasmic reticulum (ER) protein, calreticulin (CALR), at the cell surface, release of the chromatin protein high-mobility group box 1 (HMGB1), and ATP to the extracellular space [109,111]. This evidence concerns the gene CALR and neoplasm.