FAU researchers have effectively knocked out the MBLAC1 gene in mice. It has been shown that the human MBLAC1 protein binds directly to ceftriaxone (CEF), which is known to interfere with the activity and addictive properties of several commonly abused drugs, potentially curbing drug-seeking behavior. Thus, mice given cocaine are extremely hyperactive compared to normal mice, where the hyperactivity can be blocked by administering CEF. The mice that lack the MBLAC1 gene do not see the CEF-induced block of hyperactivity caused by cocaine. Thus, it can be determined that MBLAC1 is essential for cocaine-induced hyperactivity, and the model is broadly applicable for studies involving cocaine. This model system is valuable for studying the interplay between CEF and the dopamine-dependent physiological effects of drugs.