Selective FGFR4 targeting has been shown to reduce adverse effects, and the simultaneous targeting of FGFR4 and other receptor tyrosine kinases (RTKs) has been shown to indirectly enhance anti-tumor activity through normalization of the tumor microenvironment (Repana and Ross, 2015; Katoh, 2016). The gene discussed is FGFR4; the disease is neoplasm.