Intensive necrosis‐related death frequently causes immunogenic cell death (ICD);[23, 24] therefore, we evaluated damage‐associated molecular patterns (DAMPs), which correspond to ICD activities, after LAA treatment, including adenosine triphosphate (ATP) secretion, high mobility group protein B1 (HMGB1) release, and calreticulin (CRT) exposure.[25] The LAA‐treated KPC cells showed a 41.5‐fold higher level of ATP secretion and an 8.2‐fold higher level of HMGB1 release than the EtOH‐treated cells (Figure 3C,D). This evidence concerns the gene CALR and impulse control disorder.