Given the extensive cross-talk of the AhR with other oncogenic signaling pathways (including, e.g., PI3K/Akt, c-myc or Wnt/β-catenin-dependent signaling), there are multiple unknown factors, which may determine tumor suppressor or oncogenic role of AhR in a given tissue/cell-specific context [37,38,39]. This evidence concerns the gene AHR and neoplasm.