By using transgenic mice models (Hupki mice, human p53 knock-in), a previous study found that without any mutations in p53, Hupki mice were more susceptible to AFB1 exposure and subsequent formation of cancer than the mice with wild-type murine p53, thus there would be other ways of inactivation of p53 found in human exposure to AFB1 that may accelerate the transition of carcinoma [33]. The gene discussed is TP53; the disease is cancer.