Recently, we showed that p16INK4a-deficiency in murine bone marrow-derived macrophages inhibits inflammatory JAK2-STAT1 signaling, promoting the polarization into alternatively activated (M2) macrophages [15], which have been shown to protect against the development of obesity-induced glucose intolerance and insulin resistance [16]. The gene discussed is CDKN2A; the disease is Glucose intolerance.