We recently studied the possible role of Fhit in paclitaxel resistance with regard to ANXA4 overexpression; we demonstrated that, while ANXA4 is overexpressed and located to the inner side of plasma membrane in Fhit-negative lung cancer cells treated with paclitaxel, virally-mediated Fhit overexpression restores sensitivity to paclitaxel both in vitro and in vivo by delocalizing ANXA4 to cytosol [19]. Here, FHIT is linked to lung carcinoma.