Once hailed as a breakthrough in psoriasis research, the imiquimod (IMQ) mouse model is now overused, inconsistently applied, and increasingly disconnected from human disease. Nearly a decade after our initial critique, the field remains reliant on a tool that models acute, innate inflammation rather than chronic, adaptive immunity. In this paper, we revisit the limitations of the IMQ model, highlighting methodological drift, poor transcriptomic overlap with psoriasis, and the illusion of mechanistic discovery. We argue that progress in psoriasis research now depends on moving beyond this model toward more faithful systems that reflect the complexity of human disease.
