p62‐deficient mice developed obesity, insulin resistance, and fatty liver spontaneously in their later lives.[56, 57] p62 was shown to attenuate adipogenesis by inhibiting ERK signaling and macrophage inflammation in WAT while potentiating thermogenesis in BAT.[58] Meanwhile, p62 is essential for maintaining leptin sensitivity in the brain to control food intake.[59] Our study, for the first time, demonstrated that p62 is critical for modulating the Chchd10 reduction‐mediated adaptive response in white adipocytes by activating NRF2 activity. The gene discussed is NFE2L2; the disease is obesity disorder.