Patients with previously reported POU-homeodomain-truncating variants clinically presented with autosomal recessive early-onset and severe TSH, GH, and PRL deficiencies [5,31,32,33], similar to the clinical course observed in our patients, which supports the pathogenic nature of the c.744-5_749del11bp variant. The gene discussed is PRL; the disease is hyperinsulinemic hypoglycemia, familial, 4.