Candida albicans (C. albicans) is the most prevalent fungal species in humans, normally found on the mucosal surfaces of the body. In most individuals, this fungus resides as a lifelong and harmless commensal and is a member of the very few pathogens causing disease. Under certain conditions, C. albicans can induce infections that range from superficial and dermal infections to life-threatening systemic infections. Several activities identified contribute to the pathogenic potential of this fungus including molecules mediated adhesion and invasion into host cells, the yeast-to-hypha transition, the secretion of hydrolases, phenotypic switching, and other attributes. Host defense against C. albicans depends on a finely tuned implementation of immune responses, and central to this protection is the adaptive Th1 and Th17 cellular reaction. FcγRI, synonymously also referred to CD64, is a membrane spanning protein of 72 kDa and belongs to the immunoglobulin (Ig) supergene family. It has three extracellular Ig-like domains and is the only receptor that can efficiently bind monomeric IgG and aggregated IgG17. Hence, FcγRI is known to functions as a high-affinity Fcγ receptor where exists other two members FcγRII (CD32) and FcγRIII (CD16), but with low affinity. In humans, FcγRI is constitutively expressed on monocytes/macrophages, myeloid precursors, as well as follicular dendritic cells and its expression can also be induced on polymorphonuclear neutrophils via IFN-γ or G-CSF. Now, FcγRI is considered a great monocyte/macrophage-associated marker, normally used in flow cytometry (FCM) to identify leukemias with myelomonocytic differentiation.