Additionally, work by Dorfman et al. [51] suggests that for males, HED-induced microglial activation may be a compensatory response to blunted CX3CL1-CX3CR1 signaling and reduced pro-opiomelanocortin (POMC) neuron activation in the hypothalamus, while females retain this interaction and are subsequently protected from DIO [48,52]. Here, CX3CR1 is linked to hypohidrotic ectodermal dysplasia.