Cellular HK2 suppresses the mitochondrial translocation of the proapoptotic proteins BAD and BAX and inhibits CASP3 activation.65 Recently, HK2 degradation has been reported to cause mitochondrial damage, which in turn triggers CASP3 cleavage and subsequent GSDME-dependent pyroptotic tumor cell death.66 Importantly, all these physicochemical alterations in tumor cells were more pronounced following NanoTAC (+L) treatment than in the NanoTAC (−L) or VPF (+L) groups. The gene discussed is CASP3; the disease is neoplasm.