We further show that concomitant targeting of FGFR1/PLK1 adaptively evokes autophagy that limits the cytotoxicity of the combination treatment and that abrogation of protective autophagy fully releases the therapeutic potential of FGFR1/PLK inhibitor therapy, leading to greater efficacy and limited toxicity in preclinical cancer models. The gene discussed is FGFR1; the disease is cancer.