During this funding period, we investigated the levels of resistance in field populations of the Asian citrus psyllid (ACP) in commercial groves across central and southern Florida to six classes of insecticides and compared those results to previous years. In addition, we determined the baseline levels to one new chemistry, flupyradifurone, a butenolide agonist that acts on the insect nicotinic acetylcholine receptor, the same target as the neonicotinoids, imidacloprid, thiamethoxam and clothianidin. In years 2009 ‘ 2012, a decrease in susceptibility to several major classes of insecticides was observed in field ACP. In contrast, surveys conducted in 2013 and 2014 showed the return of the LD50 response in field psyllids to be equal to that of the reference laboratory strain. However, examination of the probit lines from the dose-response of field psyllids compared to laboratory strain, and with one another, revealed significant differences in response to insecticidal treatment for several populations for a number of the insecticides tested. In these studies, and those of prior funding periods, four fundamental determinations were made: (1) the enzymatic profile of detoxifying enzymes of ACP is diverse, robust and responsive. It is well documented that the evolutionary dynamic of plant-feeding insects in response to allelochemicals produced by their host plants has led to diverse enzymatic systems by the insects to detoxify the protective toxins produced by plants, and ACP appears to be no exception, (2) the insecticidal response of ACP is dynamic, showing potential for resistance against all major classes of insecticides currently used to control this insect pest, and that insecticidal response can return to basal levels based on LD estimates, (3) based on the analysis of probit lines, it appears that differences between populations of ACP exist at the genetic/enzymatic levels, potentially leaving some populations ‘primed’ for resistance with pressure from insecticidal exposure and (4) an LD estimate, whether it be LD50, LD75, or LD95, is probably not an appropriate metric alone to monitor for resistance in field populations of ACP. This last finding is of particular importance because as was discovered in these studies, differences in insecticidal response between populations in the last two years were only apparent by probit analysis. Given how quickly ACP can develop resistance, it is imperative to be using the most sensitive method for detection as possible. Because we did not find resistant populations during this funding period in which to study the biochemical mechanisms underlying resistance, three attempts were made to develop resistant colonies in-house with no success. However, given that the resistance induced in laboratory colonies is typically polygenetic, whereas the resistance observed in field populations is usually monogenetic, it is unlikely that the mechanisms induced in laboratory insects would be representative of the mechanism that would be observed in the field. Instead of continuing to attempt to develop a resistant colony to study insecticide resistant mechanisms in ACP, we concentrated on characterizing the voltage-gated sodium channel, the target of pyrethroids. This channel is well-known for target-site mutations that result in reduced binding of the insecticide to its target in a wide diversity of insects. We found that ACP is no exception, and that there is potential for the target to become insensitive to pyrethroids through known mutations. In particular, ACP has potential for two particular single-nucleotide polymorphisms that would result in target-site insensitivity for two of the most effective kdr mutations known. Given the wide-spread nature of these mutations within insect species, including other Hemipterans, we conclude that pressure from pyrethroids would result in target-site insensitivity, resulting in the reduced efficacy of this important insecticidal chemistry.