Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by activating β2 and β3 subunit containing channels of the GABA A receptor complex (a different binding site than benzodiazepines), and by stimulating the production of GABA(A) active neurosteroids that act in conjunction with etifoxine's direct effects.  This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites;  however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil . 
The pharmacological actions of benzodiazepines at the GABA A receptor are similar to those of neurosteroids . Neuroactive steroids are positive allosteric modulators of the GABA A receptor, enhancing GABA function and in turn have effects on mood and other functions. Many benzodiazepines ( diazepam , medazepam , estazolam , temazepam , flunitrazepam and nitrazepam) potently inhibit the enzymes involved in the metabolism of neurosteroids. The tetrahydroxazole ring that cloxazolam and oxazolam have decreases the inhibitory potency of benzodiazepines on neurosteroids. Thus there could be subtle differences between cloxazolam and other benzodiazepines.  However, because the parent prodrugs of cloxazolam and oxazolam were tested rather than the active metabolites, this is purely speculative.