Upon ligand binding, the PPARα forms a heterodimer with retinoid X receptor α, which binds to peroxisome proliferator response elements within the FADS2 promoter, thereby modulating FADS2 transcription and the subsequent biosynthesis of LC‐PUFAs.[27, 33] However, whether this regulatory axis operates under inflammatory conditions in keratinocytes, particularly in psoriasis, remains unclear. Here, FADS2 is linked to psoriasis.