This hypothesis is based on several sets of data: 1) proinflammatory M1-MF accumulate in AT during obesity, while their transformation to M2-MF aleviate obesity [4, 5, 31];2) plasmids can rather easily penetrate to bone marrow upon i.m. injection [32] [33] where AT-associated MF are generated from monocytes [34]; 3) monocytes (M0) and MF, in particular, M2-MF, can migrate from bone marrow to the sites of inflammation [35, 36]; 4) p62 overexpression in MF can inhibit their proinflammatory state (i.e. generation of proinflammatory cytokines) [37]. This evidence concerns the gene SQSTM1 and obesity disorder.