SOCS3 and atherosclerosis: During early phases of atherosclerosis, STAT3 activation represses SOCS3 levels that, in turn, increases resistin, cytokine, and reactive oxygen species (ROS) production depending on NADPH oxidase (by increased NOX1 expression) (Gan et al., 2013; Barrett et al., 2019), while the overexpression of SOCS1 represses ROS generation by inhibiting NOX expression caused by the upstream inactivation of JAK2, STAT1, and phosphoinositide 3-kinase (PI3K) (Hernández-Vargas et al., 2005; Ortiz-Muñoz et al., 2009; Recio et al., 2015).