## 1 Introduction  
The ongoing global intensification of wheat production will likely be accompanied by rising pressure of Fusarium disease [1]. The fungal genus _Fusarium_ that was introduced by German mycologist [PERSON] in 1809 is the single major cause of several plant diseases, including Fusarium Head Blight (FHB). This plague has become one of the most important cereal diseases worldwide and evidence suggests that the likelihood of FHB epidemics has increased over the past century. Pandemic lines of _Fusarium graninearum_ have augmented disease development at an accelerated rate, thus inducing large-scale outbreaks and widespread mycotoxin contamination [2; 3; 4; 5; 6]. Although significant effort has been made to control FHB and its persistent mycotoxins (e.g., deoxynivalenol- DON, zearalenoen-ZEN) in staple cereal crops, food and feed, a holistic effective management of FHB remains a challenging task for numerous innovative investigations [7]. Nowadays, assembling FHB damage data, using algorithms, and correlating predictive computational models are being explored to achieve a predictive accuracy of FHB epidemics [8] and to develop strategies for reducing risk of mycotoxins in wheat and other small grain cereals [9]. The ultimate goal is to achieve genetic gains in agronomic and selected end-use quality traits in wheat worldwide [10] to feed the growing human population. Since Fusarium Head Blight, commonly called scab, is a major pest to wheat crops, breeders strive to find achievable solutions by producing wheat varieties with resistance genes. Indeed, the plant defense responses to _Fusarium_ have been thoroughly explored,thus genomic selection in cereals has resulted in improved crop resistance which has now surpassed the efficiency of the traditional phenotypic selection in controlling FHB [1,11]. However, breeding against FHB seems to be hampered by the limited variation in the elite gene pool and difficulties in efficiently combining the numerous small-effect resistance quantitative trait loci (QTL) in the same crop line [11]. In addition to this, while historic breeding panel enables high-resolution mapping of FHB resistance QTLs [12], the _Fusarium_ infection-induced metabolic changes in different cereal varieties associate with different physiological, metabolic and phytohormonal network-related resistance [13, 14, 15]. Even with all this information, the shifts in crop defense responses have not yet been exploited for an integrated scientific strategy or management approach in controlling FHB. Furthermore, despite multiple genomics and functional traits [16,17] and their relation to the evolution of disease resistance in cereals [18], it is still unclear how resistance works. Even though it is not clearly known if other plant associated traits such as microbiome-based wheat characteristics are connected to host resistance, it is believed that the microbiome as the plant's second genome can reduce Fusarium virulence [19]. Studies have found that the microbiome of wheat can disable Fusarium pathogen infection [20] or can confer resistance [21] and so without genetic modifications. In addition, _Fusarium_ whole genome and specifically its pathogenome features have been targeted to reveal gene sequences, gene order, gene clusters, regulatory sequences, and other genomic organisational landmarks. It is possible that these revelations can provide a better understanding of the complex dynamics of host-microbe interactions that lead to diseased versus healthy plants [22]. From the pathogen perspective, virulence mechanisms, such as the production of toxins and virulence proteins, as well as pathogen reproduction and survival, have also been studied in connection to climate change [23]. On the other hand, microbiologists and plant pathologists argue that a better understanding of cereal host genetics-Fusarium genetics-beneficial microbes interactions is possible by looking more closely at FHB from a microbiome perspective [24].