We registered the down-regulation of TNFRSF1A, especially in sarcomatoid and biphasic cell lines; this could be a mechanism, induced by guadecitabine, to impair tumor progression and to avoid the recruitment of immunosuppressive cells, that act as a barrier to cancer immunotherapy, also taking into consideration the down-regulation of the expression of IL17A-specific mRNA observed in the aforementioned phenotypes. Here, TNFRSF1A is linked to neoplasm.