Thus, fitting all these evidences in the proposed hypothetical model (Figure 9), it can be suggested that insulin signaling may crosstalk with Wnt signaling, due to the existence of common downstream target genes, the shared negative mediator GSK3B, and insulin resistance are capable of explaining the association of T2D co-occurrences with other inflammatory disease like HT, and OBS. The gene discussed is GSK3B; the disease is hematocrit.