Additionally, STAT3 has been shown to act also as a transcriptional repressor of p53 [50] that, apart from its cell-autonomous effects, activates the innate immune response against cancer cells stimulating the expression of ULPB2 [51], in human tumor cells of different origin and so, the lower level of active STAT3 found in low-CB1-expressing tumor cells may be responsible of a major amount of this immunogenic ligand on their cell surface. Here, CNR1 is linked to neoplasm.