It seems that HB cells have no possibility of becoming resistant to NK-1R antagonists since in HB cells the tr-NK-1R isoform is continuously up-regulated (the truncated isoform could be responsible for a constitutive growth stimulus) and, for this reason, the antitumor effect of the NK-1R antagonists is linked to the differential expression of the NK-1R (truncated and full isoforms) in cancer cells. The gene discussed is TACR1; the disease is cancer.