We therefore propose that, in an inflammatory-hypoxic microenvironment marked by high levels of HIF1A-KDM5C-IL6, tumor cells may dedifferentiate via a survivin-dependent pathway and acquire a particular stem-like phenotype marked by a high level of NANOG expression and associated, in turn, with high p53 levels (Figure 7A). Here, HIF1A is linked to neoplasm.