Elevated levels of CRT mRNA in different tumor types correlate with inferior clinical prognoses.[186] Mechanistically, CRT triggers the PI3K and ERK pathways with the assistance of Galphai2 proteins, promoting tumor cell proliferation and survival.[185] The tumorigenic impact of CRT is further linked to diminished cell adhesion and immune evasion through compromised MHC class I antigen presentation.[191, 192] Overall, selective phagocytosis of nonapoptotic tumor cells proves advantageous for tumor therapy, while phagocytosis of apoptotic cells yields contrasting effects. The gene discussed is CALR; the disease is neoplasm.