That there is an epigenetic component is not what was contentious. My point being it is unknown which mechanism in the temperature-signal pathway is the root of TSD. KDM6B is proven to be a vital component in the epigenetic expression of DMRT1 but what triggers KDM6B? That is unexplained.

Also, I do admit "in humans, all babies start off development as females." is a bit of an exaggeration, but it is not incorrect. As seen in AIS individuals, as I highlighted in my post, without male differentiating hormones, human bodies, for the most part, develop phenotypically into female presenting bodies. So much so that prior to modern times and ready genotyping, the most common diagnoses of AIS occurred in mid to late puberty when the individual did not start menses or develop other secondary sex characteristics.

Many male organs are direct descendants/adaptations of female organs, the differentiation of which occurs only in the presence of male differentiation hormones.