it is unlikely a GIRK mutant will be identified that is deficient in PIP2 binding but has normal alcohol activation. A related question is whether a point mutation will be identified that creates an alcohol resistant GIRK channel that retains Gβγ activation. Lastly, it is unknown what determines the subtle differences in alcohol activation of GIRK channels composed of different subunits (Kobayashi et al., 1999; Lewohl et al., 1999). Thus, any therapeutic strategy to treat alcohol addiction and abuse will need to take into account these remaining questions.
