[7][8] The mRNA of the first isoform, RORγ is expressed in many tissues, including thymus, lung, liver, kidney, muscle, and brown fat.

Absent protein in previous studies may be due to the high amplitude circadian rhythm of expression of this isoform in some tissues.

This protein can bind to and activate the promoter of the ARNTL (BMAL1) gene,[15][22] a transcription factor central to the generation of physiological circadian rhythms.

Also, since the levels of RORγ are rhythmic in some tissues (liver, kidney), it has been proposed to impose a circadian pattern of expression on a number of clock-controlled genes,[14] for example the cell cycle regulator p21.

Importantly, the deletion of ARNTL in ILC3s using a RORc promoter disrupted enteric defence, reinforcing the role of clock machinery in the control of RORγt.

Consequently, removing the metabolic ground product for retinoic acid, vitamin A, from the diet of pregnant mice resulted in lower embryonic LTi cell differentiation, leading to smaller lymph nodes in the adult offspring and finally resulting in lower capabilities to clear a virus.

[6] Despite the pro-inflammatory role of RORγt in the thymus, it is expressed in a Treg cell subpopulation in the colon, and is induced by symbiotic microflora.

Abrogation of the gene's activity generally increases type 2 cytokines and may make mice more vulnerable to oxazolone-induced colitis.