These AMH oxygen-generating nanophotosensitizers were found to trigger apoptosis, CALR exposure, and DC maturation in vitro, as well as release MnO2 in the microenvironment of CT26 tumors upon NIR irradiation, thus triggering sufficient oxygen production to relieve tumor hypoxia and inducing a peritumoral immune response in vivo [98]. The gene discussed is CALR; the disease is neoplasm.