TLR7 agonists have been shown to shift macrophages toward an elevated M1/M2 ratio in psoriatic skin.[7, 15] A recent study identified TASL as an essential adaptor protein that mediates IRF5 activation downstream of TLR7–9 signaling, functionally analogous to the IRF3 adaptors STING, MAVS, and TRIF.[16] SLC15A4 has been reported to recruit TASL to the endolysosome, a prerequisite for IRF5 activation.[16, 17, 18, 19] However, the regulatory mechanisms that govern the TLR7–TASL–IRF5 axis in psoriasis remain unclear. The gene discussed is IRF5; the disease is psoriasis.