Together with previously published results that reduced CHFR expression in lung cancer is associated with improved survival following platinum taxane based therapy [6] and that taxane sensitivity is increased in gastric [1]-, colon [2]- and cervical cancers [22] in which CHFR is silenced epigenetically, we proposed a model in which pharmacologic inhibition of the CHFR-PARP1 interaction with subsequent loss of CHFR and disruption of antephase checkpoint function helps to overcome intrinsic taxane resistance across a wide spectrum of different tumor types (Figure 7). The gene discussed is CHFR; the disease is lung cancer.