To understand whether alterations in Pc-binding at specific target genes may contribute to tumour phenotypes in scrib1 disc, we performed a three-state hidden Markov model (HMM) analysis of Pc-binding at individual GATC fragments to define ‘depleted’, ‘intermediate’ and ‘enriched’ Pc-binding states and analysed transitions between these states when comparing scrib1 to WT WIDs (see Experimental procedures, Additional file 1: Fig. S4B, Additional files 2: SF2 and 3: SF3) [26, 32–35]. The gene discussed is SCRIB; the disease is neoplasm.