Despite the focus on a single animal model and cell culture models, this study revealed several key findings: First, defective CMA was observed in IMQ-induced psoriasiform lesions and IMQ-treated keratinocytes; Second, activation of CMA significantly mitigated IMQ-induced psoriasiform lesions; Third, activation of CMA in keratinocytes benefited for the regulation of keratinocyte proliferation, differentiation, and cytokine secretion; Forth, CMA-mediated degradation of TLR7 contributed to the inhibition of the TLR7-NF-κB signaling pathway implicated in psoriasis. The gene discussed is NFKB1; the disease is psoriasis.