Resistance to herbicides can be based on one of the following biochemical mechanisms: 
* Target-site resistance: In target-site resistance, the genetic change that causes the resistance directly alters the chemical mechanism the herbicide targets.  The mutation may relate to an enzyme with a crucial function in a metabolic pathway, or to a component of an electron-transport system. For example, ALS-resistant weeds developed by genetic mutations leading to an altered enzyme. Such changes render the herbicide impotent. Target-site resistance may also be caused by an over-expression of the target enzyme (via gene amplification or changes in a gene promoter).  A related mechanism is that an adaptable enzyme such as cytochrome P450 is redesigned to neutralize the pesticide itself.
* Non-target-site resistance: In non-target-site resistance, the genetic change giving resistance is not directly related to the target site, but causes the plant to be less susceptible by some other means. Some mechanisms include metabolic detoxification of the herbicide in the weed, reduced uptake and translocation, sequestration of the herbicide, or reduced penetration of the herbicide into the leaf surface. These mechanisms all cause less of the herbicide's active ingredient to reach the target site in the first place.
The following terms are also used to describe cases where plants are resistant to multiple herbicides at once:    
* Cross-resistance: In this case, a single resistance mechanism causes resistance to several herbicides. The term target-site cross-resistance is used when the herbicides bind to the same target site, whereas non-target-site cross-resistance is due to a single non-target-site mechanism (e.g., enhanced metabolic detoxification) that entails resistance across herbicides with different sites of action.
* Multiple resistance: In this situation, two or more resistance mechanisms are present within individual plants, or within a plant population.