Model depicting a putative role for Gα_i1 in weak agonist-induced signal transduction. This model incorporates the model put forward by Jin and Kunapuli3 stating that coactivation of G_i- and G_q-coupled signaling pathways are necessary for weak agonist-induced platelet aggregation. For example, with ADP and adrenaline, this G_i component is provided following activation of Gα_i2 and Gα_z, respectively. Here we propose that following agonist receptor coupling, activation of either Gα_i2 or Gα_z may require priming by Gα_i1, possibly in a c-Src–dependent manner, to regulate effectors such as adenylate cyclase or those involved in the activation of α_IIbβ₃. See “Discussion” for further details.