A biotype of green foxtail found in Spain exhibited cross-resistance among acetyl-CoA carboxylase (ACCase)–inhibiting herbicides. Field doses that totally inhibited shoot fresh weight in the susceptible (S) biotype were determined for six aryloxyphenoxypropionates (clodinafop, diclofop, fenoxaprop-P, fluazifop-P, haloxyfop-P, and propaquizafop) and six cyclohexanediones (clefoxydim, clethodim, cycloxydim, sethoxydim, tepraloxydim, and tralkoxydim). The resistant (R) biotype showed cross-resistance to all herbicides except fenoxaprop-P, propaquizafop, clefoxydim, and tepraloxydim. There were no differences in the absorption, translocation, and metabolism of [14C]diclofop between the S and R biotypes. On the basis of herbicide dose that inhibited ACCase activity by 50% (I50 values), ACCase of the R biotype was 5.8-, 13.9-, 20.0-, 102.4-, 416.7-, and 625.0-fold less sensitive to clethodim, haloxyfop, diclofop, fluazifop, cycloxydim, and sethoxydim, respectively, than that of the S biotype. Two multifunctional ACCase isoforms (ACCase I and ACCase II) were purified partially and separated. ACCase II was highly resistant to diclofop acid in both biotypes, with I50 values ranging between 92 and 95 μM. However, the I50 values observed for ACCase I revealed that the R biotype was 30.8-fold less sensitive to diclofop than the S biotype. These results suggest the mechanism of resistance in green foxtail to diclofop relates to an altered ACCase I isoform.