Experimental evidence has shown that Flt3L-deficient models exhibit reduced cDC1 numbers and diminished IL-12 levels,[39] whereas exogenous Flt3L administration activates mitogen-activated protein kinases and modulates intestinal immunity.[40] This mechanism aligns with the role of Flt3L in enhancing antitumor responses during cancer immunotherapy,[41] indicating that its immunomodulatory functions are conserved across pathological contexts. Here, WNK2 is linked to cancer.