Our results showed that unlike directly inhibiting HSP90 ATPase in the NTD, NB suppressed the expression of HSP90AB1 and blocked the HSP90‐CDC37‐client chaperone cycle, leading to inactivation of STAT3 and Akt which play a pivotal role in psoriasis.[46, 47] This selective modulation of HSP90 kinase clients, rather than non‐selective inhibition of all the client proteins, could serve as a potential alternative therapeutic strategy for psoriasis. This evidence concerns the gene AKT1 and psoriasis.