The development of resistance to acequinocyl was found in the population of the twospotted spider mite, Tetranychus urticae, collected from rose greenhouses in Gimhae, Gyeongnam province in January 2001. This pest is reared on 5 years treated with acequinocyl (over 200 times), and increased 87.8 folds in resistance as compared to susceptible strain (S). Inheritance of acequinocyl resistant strain (R) and cross resistance of this strain to 8 acaricides against T. urticae adults and eggs was investigated. There were differences of susceptibility in the acequinocyl concentration-mortality relationships in $F_1$ progenies obtained from reciprocal cross with the S and R strain ($S(female){ imes}R(male)$, $R(female){ imes}S(male)$). Degrees of dominance were -0.75, -0.57 in $F_1$ progenies of adult and egg of $S(female){ imes}R(male)$. Inheritance in $F_1$ progenies of $S(female){ imes}R(male)$ was incomplete recessive. Degree of dominance were 0.81, 0.45 in $F_1$ progenies of adult and egg of $R(female){ imes}S(male)$, respectively. These results suggest that inheritance of acequinocyl resistance is controlled by a complete dominance. The R strain exhibited cross resistance of 1.1 and 0.9 fold to amitraz, bifenazate, and negatively correlated cross resistance of 0.08 fold to emamectin benzoate in adult females. The R strain showed cross resistance of 37.7, 14.0, and 26.2 fold to amitraz, milbemectin and spriodiclofen in eggs, respectively. Particularly it showed high levels of cross-resistance to pyridaben with 6538.3 fold. These chemicals showed negatively correlated cross-resistance exhibited 0.4, 0.3, and 0.2 fold to ahamectin, bifenazate, and emamectin benzoate in eggs.