Whilst the involvement of JAK–STAT signalling has not been comprehensively examined in polarity-impaired mouse models of cancer or in human cancer [93,94], cooperation between RAS–MAPK and JAK–STAT signalling has been noted in hepatocellular carcinoma [95], and more recently a conserved cooperation between RAS–MAPK and JAK–STAT signalling was observed in the development of radiation resistance in RAS-driven tumor models [96]. This evidence concerns the gene SOAT1 and neoplasm.