Thus, perhaps on cells which developed resistance to GEM/NAB in presence of CM-HMC-1, a complex autocrine signalling loop occurred which started with the activation of PAR-2 by tryptase and involved the TGF-β receptor and maybe other tyrosine kinase receptors, through transactivation, and this has led to TGF-β1 release, PAR-2 increased expression and ERK signalling activation, which ultimately drove tumor cells’ proliferation and resistance to treatment. The gene discussed is NTRK1; the disease is neoplasm.