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The immunoinflammatory response plays a prominent role in driving atherosclerotic lesion development, progression, and complications (Binder et al., 2002; Hansson and Libby, 2006; Tedgui and Mallat, 2006; Weber et al., 2008). Defining the direct roles of specific immune regulatory pathways in the modulation of ath erosclerosis is certainly of considerable interest (Tedgui and Mallat, 2006). Suppressor of cytokine signaling (SOCS) pro teins are key physiological regulators of both innate and adaptive immunity, and control the development of various immunoinflammatory diseases (Yoshimura et al., 2007). SOCS3 is ex pressed in atherosclerotic lesions, and the cur rent paradigm suggests an atheroprotective role through inhibition of STAT3 signaling and the suppression of proinflammatory responses (Tang et al., 2005; Gharavi et al., 2007; OrtizMuñoz et al., 2009). However, its direct role in the control of the immune response of atheroscle rosis is still largely unknown. Recent studies have addressed the role of T cell–specific SOCS3 expression on T cell differentiation and cytokine production. In triguingly, one study reported preferential Th3 and/or Tr1like differentiation and reduce