As shown in Figure 6C, when compared to normal human retina, iPSC-derived photoreceptor precursor cells from a normal control and a separate RP patient with known disease-causing mutations and pathophysiology (MAK associated RP caused by nonsense mediated decay of the transcript), the proband was found to have increased expression of the markers GRP78 and GRP94 indicative of protein misfolding and subsequent ER stress (Obeng et al., 2006; Lind et al., 2013). The gene discussed is MAK; the disease is retinitis pigmentosa 1.