Malaria is a significant public health threat of the tropics, caused by Plasmodium parasite and vectored by the female Anopheles mosquitoes. An. gambiae complex is the most prevalent of all Anopheles species complexes present in tropical Africa. Principal vector control measures include indoor residual spraying and long-lasting insecticide-treated nets. These have been challenged by the emergence and spread of insecticide resistance at their target sites particularly in An. gambiae sensu lato due to insecticide resistance markers, a specific genetic variation that confers resistance to the vector aiding in tracking insecticide resistance spread and development of targeted control strategies. Recent studies have reported diverse susceptibility patterns of the An. gambiae complex to new generation insecticides broflanilide, chlorfenapyr, clothianidin, and pyriproxyfen which employ distinct modes of action and do not show cross-resistance with older insecticides. The mechanisms underlying insecticide resistance encompass reduced target-site sensitivity and the upregulation of enzymatic detoxification pathways. Genetic markers that include knockdown resistance (kdr), dieldrin resistance (rdl), and acetylcholinesterase-1 (ace-1R) are the point mutations at loci 1014, 296 and 119 of Vgsc, rdl and AcheE-1 genes, respectively, indicating reduced insecticide susceptibility. However, there is dearth of data and paucity of information on insecticide resistance markers. The detection of these genetic markers enables the informed selection of alternative insecticides, optimizing resistance management strategies. This is critical for the strategic management of insecticide resistance, as it mitigates the potential escalation in malaria incidence and mortality that may arise if resistance is not effectively controlled. This review provides a comprehensive evaluation of insecticide resistance markers in the Anopheles gambiae, alongside an analysis of prevailing trends and projections for future developments.