Zong has been CMI Program Co-Leader since 2015. He received his PhD degree from the University of Medicine and Dentistry of New Jersey (UMDNJ) and showed that NF-B blocks apoptosis by upregulating the BCL-2 family member BFL-1/A1. He did his postdoctoral training with Craig Thompson at the University of Pennsylvania, where he showed that Bax/Bak are essential for apoptosis initiated from mitochondria and the endoplasmic reticulum. He demonstrated that DNA alkylating agents induce excessive DNA damage leading to hyperactivation of PARP, bioenergetic catastrophe, and necrotic cell death. Zong established his own laboratory at Stony Brook University in 2005 and moved to Rutgers University in 2015. He showed that chemotherapy-induced necrosis triggers anti-tumor innate immunity, that excessive autophagy facilitates tumor cell necrosis, and that PI3 kinases play differential roles in regulating autophagy. He is currently a John L. Colaizzi Professor in the Department of Chemical Biology, Ernest Mario School of Pharmacy, and is investigating the molecular regulation of the cancer cell stress response and nitrogen metabolism. He discovered that c-MYC promotes de novo glutamine synthesis to support cancer cell growth and proliferation, and that glutamine metabolism plays a critical role in the development of pancreatic ductal adenocarcinoma (PDAC) and hepatocellular carcinoma. He found that the ubiquitin E3 ligase TRIM21 plays a crucial role regulating protein and redox homeostasis, and its inhibition limits the development of hepatocellular carcinoma while mitigates cardiac injury in doxorubicin chemotherapy. Zong serves on numerous review panels at NIH study sections.